start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=11
article-no=
start-page=2261
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250531
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Automatic Code Generation Tool Using Generative Artificial Intelligence for Element Fill-in-the-Blank Problems in a Java Programming Learning Assistant System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Presently, Java is a fundamental object-oriented programming language that can be mastered by any student in information technology or computer science. To assist both teachers and students, we developed the Java Programming Learning Assistant System (JPLAS). It offers several types of practice problems with different levels and learning goals for step-by-step self-study, where any answer is automatically marked in the system. One challenge for teachers that is addressed with JPLAS is the generation of proper exercise problems that meet learning requirements. We implemented programs for generating new problems from given source codes, as collecting and evaluating suitable codes remains time-consuming. In this paper, we present an automatic code generation tool using generative AI to solve this challenge. Prompt engineering is used to help generate an appropriate source code, and the quality is controlled by optimizing the prompt based on the outputs. For applications in JPLAS, we implement a web application system to automatically generate an element fill-in-the-blank problem (EFP) in JPLAS. For evaluation, we select the element fill-in-the-blank problem (EFP) as the target type in JPLAS and generate several instances using this tool. The results confirm the validity and effectiveness of the proposed method.
en-copyright=
kn-copyright=

en-aut-name=ZhuZihao
en-aut-sei=Zhu
en-aut-mei=Zihao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FunabikiNobuo
en-aut-sei=Funabiki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MentariMustika
en-aut-sei=Mentari
en-aut-mei=Mustika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AungSoe Thandar
en-aut-sei=Aung
en-aut-mei=Soe Thandar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KaoWen-Chung
en-aut-sei=Kao
en-aut-mei=Wen-Chung
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LeeYi-Fang
en-aut-sei=Lee
en-aut-mei=Yi-Fang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Information and Communication Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Electrical Engineering, National Taiwan Normal University
kn-affil=

affil-num=6
en-affil=Department of Industrial Education, National Taiwan Normal University
kn-affil=
en-keyword=JPLAS
kn-keyword=JPLAS
en-keyword=Java programming learning
kn-keyword=Java programming learning
en-keyword=learning requirements
kn-keyword=learning requirements
en-keyword=generative AI
kn-keyword=generative AI
en-keyword=prompt engineering
kn-keyword=prompt engineering
en-keyword=quality control
kn-keyword=quality control
en-keyword=prompt optimization
kn-keyword=prompt optimization
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=21
article-no=
start-page=11479
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dennd2c Negatively Controls Multinucleation and Differentiation in Osteoclasts by Regulating Actin Polymerization and Protrusion Formation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Osteoclasts are bone-resorbing multinucleated giant cells formed by the fusion of monocyte/macrophage lineages. Various small GTPases are involved in the multinucleation and differentiation of osteoclasts. However, the roles of small GTPases regulatory molecules in osteoclast differentiation remain unclear. In the present study, we examined the role of Dennd2c, a putative guanine nucleotide exchange factor for Rab GTPases, in osteoclast differentiation. Knockdown of Dennd2c promoted osteoclast differentiation, resorption, and expression of osteoclast markers. Morphologically, Dennd2c knockdown induced the formation of larger osteoclasts with several protrusions. In contrast, overexpression of Dennd2c inhibited the multinucleation and differentiation of osteoclasts, bone resorption, and the expression of osteoclast markers. Dennd2c-overexpressing macrophages exhibited spindle-shaped mononuclear cells and long thin protrusions. Treatment of Dennd2c-overexpressing cells with the Cdc42 inhibitor ML-141 or the Rac1 inhibitor 6-thio-GTP prevented protrusion formation. Moreover, treatment of Dennd2c-overexpressing cells with the actin polymerization inhibitor latrunculin B restored multinucleated and TRAP-positive osteoclast formation. These results indicate that Dennd2c negatively regulates osteoclast differentiation and multinucleation by modulating protrusion formation in macrophages.
en-copyright=
kn-copyright=

en-aut-name=KoyanagiYu
en-aut-sei=Koyanagi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakaiEiko
en-aut-sei=Sakai
en-aut-mei=Eiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamaguchiYu
en-aut-sei=Yamaguchi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FarhanaFatima
en-aut-sei=Farhana
en-aut-mei=Fatima
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TairaYohsuke
en-aut-sei=Taira
en-aut-mei=Yohsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkamotoKuniaki
en-aut-sei=Okamoto
en-aut-mei=Kuniaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataHiroshi
en-aut-sei=Murata
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TsukubaTakayuki
en-aut-sei=Tsukuba
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=2
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=3
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=4
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=5
en-affil=Division of Cariology and Restorative Dentistry, Department of Prosthetic Dentistry, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=6
en-affil=Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Division of Cariology and Restorative Dentistry, Department of Prosthetic Dentistry, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=

affil-num=8
en-affil=Department of Dental Pharmacology, Graduate School of Biomedical Sciences, Nagasaki University
kn-affil=
en-keyword=osteoclast
kn-keyword=osteoclast
en-keyword=actin polymerization
kn-keyword=actin polymerization
en-keyword=protrusion formation
kn-keyword=protrusion formation
en-keyword=Dennd2c
kn-keyword=Dennd2c
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=22
end-page=32
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250805
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Data inventory, processing, and reporting on plant blindness among high school students in three schools in West Java
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Plant blindness is a problem related to a person's inability to realize, recognize, and know the benefits and roles of plants. After some research, there was a shift in the term, from Plant Blindness to Plant Awareness Disparity. This study aims to find out the prevalence of Plant Blindness in three high schools in West Java. The method used in this study is descriptive Cross sectional. The results of this study revealed that there were differences in the level of plant awareness in the three schools studied. One of the schools in the city of Bandung showed the highest plant awareness rate. In addition, it was also found that students who had a high level of plant awareness had a high perception of plant awareness. As a follow-up, further research can be carried out to collect more data so that it becomes a whole population. In addition, researchers can then use additional instruments so that more things can be revealed about plant blindness.
en-copyright=
kn-copyright=

en-aut-name=SorayaPuan Helwa Rezha
en-aut-sei=Soraya
en-aut-mei=Puan Helwa Rezha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SolihatRini
en-aut-sei=Solihat
en-aut-mei=Rini
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SanjayaYayan
en-aut-sei=Sanjaya
en-aut-mei=Yayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HaradaTaro
en-aut-sei=Harada
en-aut-mei=Taro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=2
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=3
en-affil=Biology Education, Faculty of Mathematics and Science Education, Universitas Pendidikan Indonesia
kn-affil=

affil-num=4
en-affil=Graduate School of Education, Okayama University
kn-affil=
en-keyword=Descriptive statistics
kn-keyword=Descriptive statistics
en-keyword=Inferential statistics
kn-keyword=Inferential statistics
en-keyword=Plant Blindness
kn-keyword=Plant Blindness
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250811
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=RNA Delivery Using a Graphene Oxide-Polyethylenimine Hybrid Inhibiting Myotube Differentiation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Graphene oxide (GO) conjugated with short polyethylenimine (PEI) chains (GO-PEI) has been designed as a candidate nanocarrier for small interfering RNA (siRNA) delivery to mammalian cells based on the efficient interaction between the positively charged GO-based platform and the negatively charged siRNA. The function and efficiency of siRNA delivery using GO-PEI were compared to those using the positive control Lipofectamine RNAiMax by analyzing the differentiation to myotubes, and myogenin gene and protein expression in C2C12 cells. RNAiMax transfection induced cellularization and reduction of both myogenin gene and protein expression, suggesting that the differentiation of C2C12 cells was triggered by gene silencing. While GO-PEI also promoted cellularization, the myogenin gene expression remained comparable to scrambled controls, whereas the protein levels were higher than those observed with RNAiMax. Mechanistically, we attributed the reduced gene silencing efficiency of GO-PEI to a poor endosomal escape, despite strong siRNA complexation. This limitation was likely due to a low buffering capacity of GO-PEI, as a significant fraction of nitrogen atoms were already protonated, reducing the availability of free amines necessary for endosomal disruption. An appropriate chemical modification to enhance siRNA release from the endosomes is therefore essential for advancing the development of GO-based platforms as versatile and efficient nanocarriers in gene therapy applications.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraKoji
en-aut-sei=Matsuura
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ReinaGiacomo
en-aut-sei=Reina
en-aut-mei=Giacomo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GaoZhengfeng
en-aut-sei=Gao
en-aut-mei=Zhengfeng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishinaYuta
en-aut-sei=Nishina
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BiancoAlberto
en-aut-sei=Bianco
en-aut-mei=Alberto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=2
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=3
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=

affil-num=4
en-affil=Research Institute for Interdisciplinary Science, Okayama University
kn-affil=

affil-num=5
en-affil=CNRS, Immunology, Immunopathology and Therapeutic Chemistry, UPR3572, University of Strasbourg, ISIS
kn-affil=
en-keyword=graphene oxide
kn-keyword=graphene oxide
en-keyword=polyethylenimine
kn-keyword=polyethylenimine
en-keyword=myotubes
kn-keyword=myotubes
en-keyword=myogenin
kn-keyword=myogenin
en-keyword=small interfering RNA
kn-keyword=small interfering RNA
en-keyword=transfection
kn-keyword=transfection
END

start-ver=1.4
cd-journal=joma
no-vol=1869
cd-vols=
no-issue=12
article-no=
start-page=130860
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250913
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The F54L mutation of Thioredoxin shows protein instability and increased fluctuations of the catalytic center
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Thioredoxin is a ubiquitous redox protein that acts as an electron donor via its conserved dithiol motif (C32GPC35), catalyzing dithiol?disulfide exchange to regulate the redox state of target proteins. It supports antioxidant defense via peroxiredoxins, facilitates DNA synthesis by donating electrons to ribonucleotide reductase, and regulates redox-sensitive signaling pathways, including those controlling transcription and apoptosis. Neuronal degeneration and chronic kidney disease have been observed in Txn-F54L mutant rats; however, the details of why the Txn mutation causes these phenomena remain unknown. The present study aimed to elucidate the functional and structural changes caused by the F54L mutation. The Thioredoxin-F54L showed less insulin-reducing activity and more thermosensitivity to denaturation in the body temperature range compared to the wild type. The crystal structure revealed that F54 forms hydrophobic interactions with the surrounding hydrophobic amino acids. In addition, molecular dynamics simulation predicts increased fluctuations around the F54L mutation and a tendency for the distance between residues C32 and C35 at the catalytic center to be widened. The increased distance between residues C32 and C35 of the catalytic center may affect the reducing activity of the enzyme on the substrate. The finding that Thioredoxin-F54L is prone to denaturation at normal body temperature may reduce the normally functioning Thioredoxin. These molecular characteristics of Thioredoxin-F54L may be related to brain and kidney disease development in the Txn-F54L rats.
en-copyright=
kn-copyright=

en-aut-name=BabaTakumi
en-aut-sei=Baba
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UenoGo
en-aut-sei=Ueno
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OheChika
en-aut-sei=Ohe
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SajiShuku
en-aut-sei=Saji
en-aut-mei=Shuku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoSachiko
en-aut-sei=Yamamoto
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoMasaki
en-aut-sei=Yamamoto
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakagawaHiroshi
en-aut-sei=Nakagawa
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkazakiNobuo
en-aut-sei=Okazaki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=Kawasaki-OhmoriIori
en-aut-sei=Kawasaki-Ohmori
en-aut-mei=Iori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakeshitaKohei
en-aut-sei=Takeshita
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=2
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=3
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=4
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=5
en-affil=Structural Biology Division, Japan Synchrotron Radiation Research Institute
kn-affil=

affil-num=6
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=

affil-num=7
en-affil=Materials Sciences Research Center, Japan Atomic Energy Agency
kn-affil=

affil-num=8
en-affil=Neutron Science and Technology Center, Comprehensive Research Organization for Science and Society (CROSS)
kn-affil=

affil-num=9
en-affil=Department of Molecular Oncology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Section of Developmental Physiology and Pathology, Faculty of Education, Okayama University
kn-affil=

affil-num=11
en-affil=Life Science Research Infrastructure Group, Advanced Photon Technology Division, RIKEN SPring-8 Center
kn-affil=
en-keyword=Txn
kn-keyword=Txn
en-keyword=Thioredoxin
kn-keyword=Thioredoxin
en-keyword=Protein instability
kn-keyword=Protein instability
en-keyword=Thermosensitivity
kn-keyword=Thermosensitivity
en-keyword=Crystal structure
kn-keyword=Crystal structure
en-keyword=Molecular dynamics simulation
kn-keyword=Molecular dynamics simulation
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=1
end-page=3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual-action intranasal oxytocin enhances both male sexual performance and fertility in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=EnomotoChica
en-aut-sei=Enomoto
en-aut-mei=Chica
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtiTakumi
en-aut-sei=Oti
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTakahiro
en-aut-sei=Yamanaka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShimadaMasayuki
en-aut-sei=Shimada
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=4
en-affil=Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University
kn-affil=

affil-num=5
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=intranasal administration
kn-keyword=intranasal administration
en-keyword=sexual behavior
kn-keyword=sexual behavior
en-keyword=sperm motility
kn-keyword=sperm motility
en-keyword=paraventricular nucleus
kn-keyword=paraventricular nucleus
en-keyword=male sexual function
kn-keyword=male sexual function
en-keyword=androgen signaling
kn-keyword=androgen signaling
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=17
article-no=
start-page=8643
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250905
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anti-HMGB1 Antibody Therapy Ameliorates Spinal Cord Ischemia?Reperfusion Injury in Rabbits
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Spinal cord ischemia?reperfusion (SCI/R) injury remains a major clinical challenge with limited therapeutic options. High-mobility group box 1 (HMGB1), a proinflammatory mediator released during cellular stress, has been implicated in the pathogenesis of ischemia?reperfusion-induced neural damage. In this study, we investigated the neuroprotective potential of the anti-HMGB1 monoclonal antibody (mAb) in a rabbit model of SCI/R injury. Male New Zealand White rabbits were anesthetized and subjected to 11 min of abdominal aortic occlusion using a micro-bulldog clamp following heparinization. Anti-HMGB1 mAb or control IgG was administered intravenously immediately after reperfusion and again at 6 h post-reperfusion. Neurological function was assessed at 6, 24, and 48 h after reperfusion using the modified Tarlov scoring system. The rabbits were euthanized 48 h after reperfusion for spinal cord and blood sampling. Treatment with anti-HMGB1 mAb significantly improved neurological outcomes, reduced the extent of spinal cord infarction, preserved motor neuron viability, and decreased the presence of activated microglia and infiltrating neutrophils. Furthermore, it attenuated apoptosis, oxidative stress, and inflammatory responses in the spinal cord, and helped maintain the integrity of the blood?spinal cord barrier. These findings suggest that anti-HMGB1 mAb may serve as a promising therapeutic agent for SCI/R injury.
en-copyright=
kn-copyright=

en-aut-name=MuraokaGenya
en-aut-sei=Muraoka
en-aut-mei=Genya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiiYasuhiro
en-aut-sei=Fujii
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuKeyue
en-aut-sei=Liu
en-aut-mei=Keyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=QiaoHandong
en-aut-sei=Qiao
en-aut-mei=Handong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WangDengli
en-aut-sei=Wang
en-aut-mei=Dengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OusakaDaiki
en-aut-sei=Ousaka
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OozawaSusumu
en-aut-sei=Oozawa
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KasaharaShingo
en-aut-sei=Kasahara
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Translational Research, Center for Innovative Clinical Medicine, Medical Development Field, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pharmacology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Medical Technology, Faculty of Science, Okayama University of Science
kn-affil=

affil-num=7
en-affil=Division of Medical Safety Management, Safety Management Facility, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Translational Research and Drug Development, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=thoracoabdominal aortic aneurysm
kn-keyword=thoracoabdominal aortic aneurysm
en-keyword=spinal cord ischemia?reperfusion injury
kn-keyword=spinal cord ischemia?reperfusion injury
en-keyword=high mobility group box 1
kn-keyword=high mobility group box 1
en-keyword=neuroprotection
kn-keyword=neuroprotection
en-keyword=blood?spinal cord barrier
kn-keyword=blood?spinal cord barrier
en-keyword=aortic surgery
kn-keyword=aortic surgery
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=
article-no=
start-page=113544
end-page=113556
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Optimized Ensemble Deep Learning for Real-Time Intrusion Detection on Resource-Constrained Raspberry Pi Devices
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The rapid growth of Internet of Things (IoT) networks has increased security risks, making it essential to have effective Intrusion Detection Systems (IDS) for real-time threat detection. Deep learning techniques offer promising solutions for such detection due to their superior complex pattern recognition and anomaly detection capabilities in large datasets. This paper proposes an optimized ensemble-based IDS designed specifically for efficient deployment on edge hardware. However, deploying such computationally intensive models on resource-limited edge devices remains a significant challenge due to model size and computational overhead on devices with limited processing capabilities. Building upon our previously developed stacked Long Short-Term Memory (LSTM) model integrated with ANOVA feature selection, we optimize it by integrating dual-stage model compression: pruning and quantization to create a lightweight model suitable for real-time inference on Raspberry Pi devices. To evaluate the system under realistic conditions, we combined with a Kafka-based testbed to simulate dynamic IoT environments with variable traffic loads, delays, and multiple simultaneous attack sources. This enables the assessment of detection performance under varying traffic volumes, latency, and overlapping attack scenarios. The proposed system maintains high detection performance with accuracy of 97.3% across all test scenarios, while efficiently leveraging multi-core processing with peak CPU usage reaching 111.8%. These results demonstrate the system�fs practical viability for real-time IoT security at the edge.
en-copyright=
kn-copyright=

en-aut-name=MusthafaMuhammad Bisri
en-aut-sei=Musthafa
en-aut-mei=Muhammad Bisri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HudaSamsul
en-aut-sei=Huda
en-aut-mei=Samsul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NguyenTuy Tan
en-aut-sei=Nguyen
en-aut-mei=Tuy Tan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoderaYuta
en-aut-sei=Kodera
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NogamiYasuyuki
en-aut-sei=Nogami
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Interdisciplinary Education and Research Field, Okayama University
kn-affil=

affil-num=3
en-affil=School of Informatics, Computing, and Cyber Systems, Northern Arizona University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Internet of things
kn-keyword=Internet of things
en-keyword=intrusion detection system
kn-keyword=intrusion detection system
en-keyword=stacked lstm
kn-keyword=stacked lstm
en-keyword=pruning model
kn-keyword=pruning model
en-keyword=optimizing model
kn-keyword=optimizing model
en-keyword=quantization model
kn-keyword=quantization model
en-keyword=raspberry pi
kn-keyword=raspberry pi
en-keyword=real-time detection
kn-keyword=real-time detection
en-keyword=apache kafka
kn-keyword=apache kafka
END

start-ver=1.4
cd-journal=joma
no-vol=149
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250426
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cerebral Braak stage and amygdala granular fuzzy astrocyte status have independent effects on neuronal 3R-tau and 4R-tau accumulations in the olfactory bulb, respectively, in cases with low to intermediate AD neuropathologic change
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyashitaAkinori
en-aut-sei=Miyashita
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishikawaNaoto
en-aut-sei=Nishikawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Okayama University Medical School
kn-affil=

affil-num=4
en-affil=Okayama University Medical School
kn-affil=

affil-num=5
en-affil=Department of Neurology, National Hospital Organization Minami-Okayama Medical Center
kn-affil=

affil-num=6
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=7
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=8
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=9
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Asymptomatic intracranial vascular lesions and cognitive function in a general population of Japanese men: Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Intracranial subclinical vessel diseases are considered important indicators of cognitive impairment. However, a comprehensive assessment of various types of vessel disease, particularly in Asian populations, is lacking. We aimed to compare multiple types of intracranial vessel disease in association with cognitive function among a community-based Japanese male population. Methods: The Shiga Epidemiological Study of Subclinical Atherosclerosis (SESSA) randomly recruited and examined a community-based cohort of Japanese men from Shiga, Japan. We analyzed those who underwent the Cognitive Abilities Screening Instrument (CASI) assessment and cranial magnetic resonance imaging/angiogram (MRI/MRA) in 2010?2015. Using MRI/MRA, we assessed lacunar infarction, microbleeds, periventricular hyperintensity (PVH), deep subcortical white matter hyperintensity (DSWMH), and intracranial artery stenosis (ICAS). We divided these subclinical cerebrovascular diseases (SCDs) into three categories according to severity. Using linear regression, we calculated the CASI score according to the grade of each vessel disease, adjusted for age and years of education. Results: In the adjusted models, CASI scores were significantly associated with both PVH and DSWMH. Specifically, multivariable-adjusted CASI scores declined across increasing severity categories of DSWMH (91.7, 91.2, and 90.4; p for trend = 0.011) and PVH (91.5, 90.4, and 89.7; p for trend = 0.006). Other SCDs did not show significant associations. In stratified analyses based on the presence or absence of each SCD, both DSWMH and PVH demonstrated significant inverse trends with CASI scores in the absence of lacunar infarcts and microbleeds and in the presence of ICAS. Additionally, among participants with PVH (+), ?moderate ICAS was significantly associated with lower CASI scores. Conclusion: PVH and DSWMH showed significant dose-response relationships with cognitive function among community-based Japanese men. These findings suggest that white matter lesions may be an important indicator of early cognitive impairment, and severe ICAS may also play a role in those with PVH.
en-copyright=
kn-copyright=

en-aut-name=ItoTakahiro
en-aut-sei=Ito
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujiyoshiAkira
en-aut-sei=Fujiyoshi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhkuboTakayoshi
en-aut-sei=Ohkubo
en-aut-mei=Takayoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ShiinoAkihiko
en-aut-sei=Shiino
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShitaraSatoshi
en-aut-sei=Shitara
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyagawaNaoko
en-aut-sei=Miyagawa
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ToriiSayuki
en-aut-sei=Torii
en-aut-mei=Sayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HisamatsuTakashi
en-aut-sei=Hisamatsu
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SegawaHiroyoshi
en-aut-sei=Segawa
en-aut-mei=Hiroyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KondoKeiko
en-aut-sei=Kondo
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KadotaAya
en-aut-sei=Kadota
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TooyamaIkuo
en-aut-sei=Tooyama
en-aut-mei=Ikuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=WatanabeYoshiyuki
en-aut-sei=Watanabe
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YoshidaKazumichi
en-aut-sei=Yoshida
en-aut-mei=Kazumichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=NozakiKazuhiko
en-aut-sei=Nozaki
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=MiuraKatsuyuki
en-aut-sei=Miura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=The SESSA Research Group
en-aut-sei=The SESSA Research Group
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=2
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=3
en-affil=Department of Hygiene and Public Health, Teikyo University School of Medicine
kn-affil=

affil-num=4
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=

affil-num=5
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=6
en-affil=Department of Preventive Medicine and Public Health, Keio University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=8
en-affil=Department of Public Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=10
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=11
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=12
en-affil=Molecular Neuroscience Research Center, Shiga University of Medical Science
kn-affil=

affil-num=13
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=14
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=15
en-affil=Department of Neurosurgery, Shiga University of Medical Science
kn-affil=

affil-num=16
en-affil=Department of Radiology, Shiga University of Medical Science
kn-affil=

affil-num=17
en-affil=
kn-affil=
en-keyword=Cognitive impairment
kn-keyword=Cognitive impairment
en-keyword=Cerebrovascular disease
kn-keyword=Cerebrovascular disease
en-keyword=Brain magnetic resonance imaging
kn-keyword=Brain magnetic resonance imaging
en-keyword=White matter lesion
kn-keyword=White matter lesion
en-keyword=Community-based population study
kn-keyword=Community-based population study
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=
article-no=
start-page=244
end-page=256
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Postnatal expression of Cat-315-positive perineuronal nets in the SAMP10 mouse primary somatosensory cortex
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Perineuronal nets (PNNs) form at the end of the critical period of plasticity in the mouse primary somatosensory cortex. PNNs are said to have functions that control neuroplasticity and provide neuroprotection. However, it is not clear which molecules in PNNs have these functions. We have previously reported that Cat-315-positive molecules were not expressed in the PNNs of the senescence-accelerated model (SAM)P10 strain model mice at 12 months of age. To confirm whether the loss of Cat-315-positive molecules occurred early in life in SAMP10 mice, we examined Cat-315-positive PNNs in the primary somatosensory cortex during postnatal development. This research helps to elucidate the function of PNNs and the mechanism of cognitive decline associated with ageing. To confirm whether Cat-315-positive PNNs changed in an age-dependent manner in SAMP10 mice, we examined the primary somatosensory cortex at 21, 28, and 56 days after birth. We compared these results with those of senescence-accelerated mouse-resistant (SAMR) mice. In SAMP10 mice, Cat-315-positive PNNs were expressed in the primary somatosensory cortex early after birth, but their expression was significantly lower than that in SAMR1 mice. Many other molecules that calibrated the PNN were unchanged between SAMP10 and SAMR1 mice. This study revealed that the expression of the Cat-315 epitope was decreased in the primary somatosensory cortex of SAMP10 mice during postnatal development. SAMP10 mice have had histological abnormalities in their brains since early life. Furthermore, using SAMP10 will be useful in elucidating the mechanism of age-related abnormalities in brain function as well as in elucidating the function and structure of PNNs.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=Ageing
kn-keyword=Ageing
en-keyword=Brain function
kn-keyword=Brain function
en-keyword=Neuroplasticity
kn-keyword=Neuroplasticity
en-keyword=Neuroprotection
kn-keyword=Neuroprotection
en-keyword=Cognitive decline
kn-keyword=Cognitive decline
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Age-related behavioural abnormalities in C57BL/6.KOR?Apoe shl mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Spontaneously hyperlipidaemic (Apoeshl) mice were discovered in 1999 as mice lacking apolipoprotein E (ApoE) owing to a mutation in the Apoe gene. However, age-related behavioural changes in commercially available Apoeshl mice have not yet been clarified. The behavioural abnormalities of ApoE-deficient mice, which are genetically modified mice artificially deficient in ApoE, have been investigated in detail, and it has been reported that they can serve as a model of Alzheimer�fs disease (AD). To understand whether Apoeshl mice can also serve as a murine model of AD, it is necessary to investigate age-related behavioural abnormalities in Apoeshl mice. In this study, we conducted a series of behavioural experiments on 7- and 11-month-old Apoeshl mice to investigate the behavioural abnormalities associated with ageing in Apoeshl mice. In this study, 7-month-old Apoeshl mice showed decreased body weight and grip strength compared to age-matched wild-type mice. In the open field test, 7-month-old Apoeshl mice showed increased anxiety-like behaviour compared to wild-type mice, whereas 11-month-old Apoeshl mice showed decreased anxiety-like behaviour. Moreover, Apoeshl mice aged 7 and 11 months had increased serum cholesterol levels. These results indicate that the behaviour of Apoeshl mice changes with age. However, 11-month-old Apoeshl mice did not show a decline in cognitive function or memory ability similar to murine models of AD. Our findings indicate that Apoeshl mice can be used to investigate the function of ApoE in the central nervous system.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyazakiTetsuji
en-aut-sei=Miyazaki
en-aut-mei=Tetsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=8
en-affil=Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=age
kn-keyword=age
en-keyword=apolipoprotein
kn-keyword=apolipoprotein
en-keyword=behavioural test
kn-keyword=behavioural test
en-keyword=central nervous system
kn-keyword=central nervous system
en-keyword=mouse
kn-keyword=mouse
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Rearing in an envy-like environment increases anxiety-like behaviour in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Interest in the societal and psychological harm caused by widespread envy and social comparison is increasing. Envy is associated with anxiety and depression, though the mechanism by which envy affects neuropsychiatric disorders, such as depression, remains unclear. Clarifying the neurobiological basis of envy�fs effects on behaviour and emotion regulation in experimental mice is essential for developing disease-prevention and treatment strategies. As mice recognize other mice in neighbouring cages, this study investigated whether they recognize neighbouring cages housed in environmentally enriched cages and suffer psychological stress due to envy. After being raised in an envy-like environment for 3 weeks, we revealed changes in the behaviour of the mice through a series of behavioural experiments. Mice raised in an envious environment showed increased body weight and anxiety-like behaviour but decreased social behaviour and serum corticosterone levels compared to control mice. Thus, mice recognize their neighbouring cages and experience psychological stress due to envy. This study revealed a part of the scientific basis for why envy increased anxiety. Using this novel experimental breeding environment, it may be possible to create an experimental animal model of anxiety disorders.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KitanoEriko
en-aut-sei=Kitano
en-aut-mei=Eriko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
en-keyword=behaviour
kn-keyword=behaviour
en-keyword=anxiety
kn-keyword=anxiety
en-keyword=mouse
kn-keyword=mouse
en-keyword=envy
kn-keyword=envy
en-keyword=rodent
kn-keyword=rodent
END

start-ver=1.4
cd-journal=joma
no-vol=2024
cd-vols=
no-issue=
article-no=
start-page=9215607
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mice Recognise Mice in Neighbouring Rearing Cages and Change Their Social Behaviour
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mice are social animals that change their behaviour primarily in response to visual, olfactory, and auditory information from conspecifics. Rearing conditions such as cage size and colour are important factors influencing mouse behaviour. In recent years, transparent plastic cages have become standard breeding cages. The advantage of using a transparent cage is that the experimenter can observe the mouse from outside the cage without touching the cage. However, mice may recognise the environment outside the cage and change their behaviour. We speculated that mice housed in transparent cages might recognise mice in neighbouring cages. We used only male mice in this experiment. C57BL/6 mice were kept in transparent rearing cages with open lids, and the cage positions were maintained for 3 weeks. Subsequently, we examined how mice behaved toward cagemate mice, mice from neighbouring cages, and mice from distant cages. We compared the level of interest in mice using a social preference test. Similar to previous reports, subject mice showed a high degree of interest in unfamiliar mice from distant cages. By contrast, subject mice reacted to mice from neighbouring cages as familiar mice, similar to cagemate mice. This suggests that mice housed in transparent cages with open lids perceive the external environment and identify mice in neighbouring cages. Researchers should pay attention to the environment outside the mouse cage, especially for the social preference test.
en-copyright=
kn-copyright=

en-aut-name=UenoHiroshi
en-aut-sei=Ueno
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakahashiYu
en-aut-sei=Takahashi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriSachiko
en-aut-sei=Mori
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MurakamiShinji
en-aut-sei=Murakami
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WaniKenta
en-aut-sei=Wani
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsumotoYosuke
en-aut-sei=Matsumoto
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshiharaTakeshi
en-aut-sei=Ishihara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medical Technology, Kawasaki University of Medical Welfare
kn-affil=

affil-num=2
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=3
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Medical Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Psychiatry, Kawasaki Medical School
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=12
article-no=
start-page=1399
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250611
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Association Between Chewing Status and Steatotic Liver Disease in Japanese People Aged ?50 Years: A Cohort Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: In this longitudinal study, the relationship between chewing status and steatotic liver disease (SLD) was examined in 3775 people aged ?50 years who underwent medical checkups at Junpukai Health Maintenance Center in Okayama, Japan. Methods: Participants without SLD at the time of a baseline survey in 2018 were followed until 2022. Chewing status was assessed by a self-administered questionnaire. The presence or absence of SLD was ascertained from the medical records of Junpukai Health Maintenance Center. Results: A total of 541 participants (14%) were diagnosed as having a poor chewing status at baseline. Furthermore, 318 (8%) participants were newly diagnosed with SLD at follow-up. In multivariate logistic regression analyses, the presence or absence of SLD was found to be associated with the following characteristics at baseline: sex (male: odds ratio [ORs] = 1.806; 95% confidence interval [CIs]: 1.399?2.351), age (ORs = 0.969; 95% CIs: 0.948?0.991), body mass index (?25.0 kg/m2; ORs = 1.934; 95% CIs: 1.467?2.549), diastolic blood pressure (ORs = 1.017; 95% CIs: 1.002?1.032), and chewing status (poor: ORs = 1.472; 95% CIs: 1.087?1.994). Conclusions: The results indicate that a poor chewing status was associated with SLD development after 4 years. Aggressively recommending dental visits to participants with poor chewing status may not only improve their ability to chew well but may also reduce the incidence of SLD.
en-copyright=
kn-copyright=

en-aut-name=IwaiKomei
en-aut-sei=Iwai
en-aut-mei=Komei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=EkuniDaisuke
en-aut-sei=Ekuni
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AzumaTetsuji
en-aut-sei=Azuma
en-aut-mei=Tetsuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YonenagaTakatoshi
en-aut-sei=Yonenaga
en-aut-mei=Takatoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TabataKoichiro
en-aut-sei=Tabata
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ToyamaNaoki
en-aut-sei=Toyama
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KataokaKota
en-aut-sei=Kataoka
en-aut-mei=Kota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaruyamaTakayuki
en-aut-sei=Maruyama
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TomofujiTakaaki
en-aut-sei=Tomofuji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

affil-num=2
en-affil=Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

affil-num=4
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

affil-num=5
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=

affil-num=6
en-affil=Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Community Oral Health, School of Dentistry, Asahi University
kn-affil=
en-keyword=oral health
kn-keyword=oral health
en-keyword=liver diseases
kn-keyword=liver diseases
en-keyword=longitudinal studies
kn-keyword=longitudinal studies
en-keyword=mastication
kn-keyword=mastication
en-keyword=physical examination
kn-keyword=physical examination
en-keyword=surveys and questionnaires
kn-keyword=surveys and questionnaires
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=S1
article-no=
start-page=7
end-page=12
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Basic biology is not just �gfor the birds�h: how avian studies have informed us about vertebrate reproduction
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Avian reproductive physiology has been studied for centuries, largely because of the importance of birds as food animals. It is likely that the ubiquity and ease of access to domesticated chickens led to them being used in some of the first experiments on transplantation of endocrine structures?in this case, the testes. Since then, study of seasonal changes in reproductive physiology (photoperiodism) in different orders of bird species has led to advances in the understanding of endocrine regulation of reproductive physiology and behavior. These include mechanisms of adult neuroplasticity, sexual selection, sperm competition, stress physiology, and circadian physiology. Here, we focus mainly on the discovery in birds of a neuropeptide named gonadotropin-inhibitory hormone that mostly has inhibitory effects on reproduction. This hormone has since been shown to exist in all mammals studied to date, including humans (it is known as RFamide-related peptide in mammals). We discuss the history and implications of avian studies on gonadotropin-inhibitory hormone/RFamide-related peptide for human reproductive biology.
en-copyright=
kn-copyright=

en-aut-name=BentleyGeorge E.
en-aut-sei=Bentley
en-aut-mei=George E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=GnIH
kn-keyword=GnIH
en-keyword=RFamide
kn-keyword=RFamide
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=7661
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240916
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurotransmitter recognition by human vesicular monoamine transporter 2
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Human vesicular monoamine transporter 2 (VMAT2), a member of the SLC18 family, plays a crucial role in regulating neurotransmitters in the brain by facilitating their uptake and storage within vesicles, preparing them for exocytotic release. Because of its central role in neurotransmitter signalling and neuroprotection, VMAT2 is a target for neurodegenerative diseases and movement disorders, with its inhibitor being used as therapeutics. Despite the importance of VMAT2 in pharmacophysiology, the molecular basis of VMAT2-mediated neurotransmitter transport and its inhibition remains unclear. Here we show the cryo-electron microscopy structure of VMAT2 in the substrate-free state, in complex with the neurotransmitter dopamine, and in complex with the inhibitor tetrabenazine. In addition to these structural determinations, monoamine uptake assays, mutational studies, and pKa value predictions were performed to characterize the dynamic changes in VMAT2 structure. These results provide a structural basis for understanding VMAT2-mediated vesicular transport of neurotransmitters and a platform for modulation of current inhibitor design.
en-copyright=
kn-copyright=

en-aut-name=ImDohyun
en-aut-sei=Im
en-aut-mei=Dohyun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=JormakkaMika
en-aut-sei=Jormakka
en-aut-mei=Mika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=JugeNarinobu
en-aut-sei=Juge
en-aut-mei=Narinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KishikawaJun-ichi
en-aut-sei=Kishikawa
en-aut-mei=Jun-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoTakayuki
en-aut-sei=Kato
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SugitaYukihiko
en-aut-sei=Sugita
en-aut-mei=Yukihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NodaTakeshi
en-aut-sei=Noda
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UemuraTomoko
en-aut-sei=Uemura
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShiimuraYuki
en-aut-sei=Shiimura
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsadaHidetsugu
en-aut-sei=Asada
en-aut-mei=Hidetsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IwataSo
en-aut-sei=Iwata
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=3
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Applied Biology, Kyoto Institute of Technology
kn-affil=

affil-num=5
en-affil=Institute for Protein Research, Osaka University
kn-affil=

affil-num=6
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=7
en-affil=Laboratory of Ultrastructural Virology, Institute for Life and Medical Sciences, Kyoto University
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=10
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=12
en-affil=Department of Cell Biology, Graduate School of Medicine, Kyoto University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=2
article-no=
start-page=53
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250606
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=An Endocrine-Disrupting Chemical, Bisphenol A Diglycidyl Ether (BADGE), Accelerates Neuritogenesis and Outgrowth of Cortical Neurons via the G-Protein-Coupled Estrogen Receptor
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Bisphenol A diglycidyl ether (BADGE) is the main component of epoxy resin and is used for the inner coating of canned foods and plastic food containers. BADGE can easily migrate from containers and result in food contamination; the compound is known as an endocrine-disrupting chemical. We previously reported that maternal exposure to bisphenol A bis (2,3-dihydroxypropyl) ether (BADGE?2H2O), which is the most detected BADGE derivative not only in canned foods but also in human specimens, during gestation and lactation, could accelerate neuronal differentiation in the cortex of fetuses and induce anxiety-like behavior in juvenile mice. In this study, we investigated the effects of low-dose BADGE?2H2O (1?100 pM) treatment on neurites and the mechanism of neurite outgrowth in cortical neurons. BADGE?2H2O exposure significantly increased the number of dendrites and neurite length in cortical neurons; these accelerating effects were inhibited by estrogen receptor (ER) antagonist ICI 182,780 and G-protein-coupled estrogen receptor (GPER) antagonist G15. BADGE?2H2O down-regulated Hes1 expression, which is a transcriptional repressor, and increased levels of neuritogenic factor neurogenin-3 (Ngn3) in the cortical neurons; the changes were significantly blocked by G15. These data suggest that direct BADGE?2H2O exposure can accelerate neuritogenesis and outgrowth in cortical neurons through down-regulation of Hes1 and by increasing Ngn3 levels through ERs, particularly GPER.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiyamaChiharu
en-aut-sei=Nishiyama
en-aut-mei=Chiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NagoshiTakeru
en-aut-sei=Nagoshi
en-aut-mei=Takeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyakoAkane
en-aut-sei=Miyako
en-aut-mei=Akane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OnoSuzuka
en-aut-sei=Ono
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MisawaIchika
en-aut-sei=Misawa
en-aut-mei=Ichika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IsseAika
en-aut-sei=Isse
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TomimotoKana
en-aut-sei=Tomimoto
en-aut-mei=Kana
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ZenshoKazumasa
en-aut-sei=Zensho
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=6
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=7
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=8
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=BADGE
kn-keyword=BADGE
en-keyword=neurite outgrowth
kn-keyword=neurite outgrowth
en-keyword=estrogen receptor
kn-keyword=estrogen receptor
en-keyword=GPER
kn-keyword=GPER
en-keyword=Hes1
kn-keyword=Hes1
en-keyword=neurogenin-3
kn-keyword=neurogenin-3
END

start-ver=1.4
cd-journal=joma
no-vol=472
cd-vols=
no-issue=
article-no=
start-page=123486
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical, neuroimaging and genetic findings in the Japanese case series of CLCN2-related leukoencephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Biallelic loss-of-function variants in CLCN2 lead to CLCN2-related leukoencephalopathy (CC2L), also called leukoencephalopathy with ataxia (LKPAT). CC2L is characterized clinically by a spectrum of clinical presentations including childhood- to adult-onset mild ataxia, spasticity, cognitive decline, and vision loss as well as typical MRI findings of symmetrical high signal intensities on the DWIs/T2WIs of the middle cerebellar peduncles (MCPs). We searched for pathogenic variants of CLCN2 in a case series of undiagnosed leukoencephalopathy accompanied by MCP signs, which led to the identification of four Japanese patients with CC2L. All the patients carried at least one allele of c.61dupC (p.Leu21Profs*27) in CLCN2, including compound heterozygosity with either the novel pathogenic variant c.983 + 2 T > A or the previously reported pathogenic variant c.1828C > T (p.Arg610*). Of note, all the four previously reported cases from Japan also harbored c.61dupC, and no reports of this variant have been documented from outside Japan. The allele frequency of c.61dupC in the Japanese population is 0.002152, raising the possibility of a relatively high prevalence of CC2L in Japan. Patients in this study developed symptoms after the age of 30, and demonstrated neurological signs including cerebellar ataxia, pyramidal signs, and mild cognitive impairment, consistent with previous reports. One male patient had two children, supporting preserved fertility, and another patient had calcifications in the cerebral and cerebellar surfaces. These findings provide valuable insights into the broader clinical and genetic spectra of CC2L in the Japanese population, and emphasize the importance of considering this disease in the differential diagnoses of leukoencephalopathy with MCP signs.
en-copyright=
kn-copyright=

en-aut-name=OrimoKenta
en-aut-sei=Orimo
en-aut-mei=Kenta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ChoTakusei
en-aut-sei=Cho
en-aut-mei=Takusei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakiyamaYoshio
en-aut-sei=Sakiyama
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SumiKensho
en-aut-sei=Sumi
en-aut-mei=Kensho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UchioNaohiro
en-aut-sei=Uchio
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatakeAkane
en-aut-sei=Satake
en-aut-mei=Akane
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakiyamaYoshihisa
en-aut-sei=Takiyama
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MatsushitaTakuya
en-aut-sei=Matsushita
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OmaeYosuke
en-aut-sei=Omae
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KawaiYosuke
en-aut-sei=Kawai
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TokunagaKatsushi
en-aut-sei=Tokunaga
en-aut-mei=Katsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Division of Neurology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Mitsui Memorial Hospital
kn-affil=

affil-num=8
en-affil=Department of Neurology, Mitsui Memorial Hospital
kn-affil=

affil-num=9
en-affil=Department of Neurology, Fuefuki Central Hospital
kn-affil=

affil-num=10
en-affil=Department of Neurology, Fuefuki Central Hospital
kn-affil=

affil-num=11
en-affil=Department of Neurology, Kochi Medical School, Kochi University
kn-affil=

affil-num=12
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=13
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=14
en-affil=Genome Medical Science Project, National Center for Global Health and Medicine
kn-affil=

affil-num=15
en-affil=Department of Precision Medicine Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=17
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=18
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=Leukodystrophy
kn-keyword=Leukodystrophy
en-keyword=CC2L
kn-keyword=CC2L
en-keyword=CLCN2
kn-keyword=CLCN2
en-keyword=MCP sign
kn-keyword=MCP sign
END

start-ver=1.4
cd-journal=joma
no-vol=219
cd-vols=
no-issue=
article-no=
start-page=104944
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202510
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Establishment of a transgenic strain for the whole brain calcium imaging in larval medaka fish (Oryzias latipes)
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=GCaMP-based calcium imaging is a powerful tool for investigating neural function in specific neurons. We generated transgenic (Tg) medaka strains expressing jGCaMP7s across extensive brain regions under the control of the gap43 promoter. Using these Tg larvae, calcium imaging successfully detected a tricaine-induced suppression of spontaneous neural activity and topographical visual responses in the optic tectum elicited by moving paramecia or optical fiber stimulation. These results indicate that our Tg medaka strains provide a versatile platform for investigating neural dynamics and their responses to various stimuli.
en-copyright=
kn-copyright=

en-aut-name=SekiTakahide
en-aut-sei=Seki
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyanariKazuhiro
en-aut-sei=Miyanari
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShiraishiAsuka
en-aut-sei=Shiraishi
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsudaSachiko
en-aut-sei=Tsuda
en-aut-mei=Sachiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakeuchiHideaki
en-aut-sei=Takeuchi
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=2
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=3
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=4
en-affil=Graduate School of Science and Engineering, Saitama University
kn-affil=

affil-num=5
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=
en-keyword=gap43
kn-keyword=gap43
en-keyword=JGCaMP7s
kn-keyword=JGCaMP7s
en-keyword=Ac/Ds
kn-keyword=Ac/Ds
en-keyword=Visuotopy
kn-keyword=Visuotopy
en-keyword=slc2a15b
kn-keyword=slc2a15b
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=77
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impact of amyloid and tau positivity on longitudinal brain atrophy in cognitively normal individuals
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Individuals on the preclinical Alzheimer's continuum, particularly those with both amyloid and tau positivity (A?+?T?+), display a rapid cognitive decline and elevated disease progression risk. However, limited studies exist on brain atrophy trajectories within this continuum over extended periods.<br>
Methods This study involved 367 ADNI participants grouped based on combinations of amyloid and tau statuses determined through cerebrospinal fluid tests. Using longitudinal MRI scans, brain atrophy was determined according to the whole brain, lateral ventricle, and hippocampal volumes and cortical thickness in AD-signature regions. Cognitive performance was evaluated with the Preclinical Alzheimer's Cognitive Composite (PACC). A generalized linear mixed-effects model was used to examine group?�~?time interactions for these measures. In addition, progression risks to mild cognitive impairment (MCI) or dementia were compared among the groups using Cox proportional hazards models.<br>
Results A total of 367 participants (48 A?+?T?+?, 86 A?+?T???, 63 A???T?+?, and 170 A???T???; mean age 73.8 years, mean follow-up 5.1 years, and 47.4% men) were included. For the lateral ventricle and PACC score, the A?+?T???and A?+?T?+?groups demonstrated statistically significantly greater volume expansion and cognitive decline over time than the A???T???group (lateral ventricle: ��?=?0.757 cm3/year [95% confidence interval 0.463 to 1.050], P?<?.001 for A?+?T???, and ��?=?0.889 cm3/year [0.523 to 1.255], P?<?.001 for A?+?T?+?; PACC: ��?=????0.19 /year [??0.36 to???0.02], P?=?.029 for A?+?T???, and ��?=????0.59 /year [??0.80 to???0.37], P?<?.001 for A?+?T?+). Notably, the A?+?T?+?group exhibited additional brain atrophy including the whole brain (��?=????2.782 cm3/year [??4.060 to???1.504], P?<?.001), hippocampus (��?=????0.057 cm3/year [??0.085 to???0.029], P?<?.001), and AD-signature regions (��?=????0.02 mm/year [??0.03 to???0.01], P?<?.001). Cox proportional hazards models suggested an increased risk of progressing to MCI or dementia in the A?+?T?+?group versus the A???T???group (adjusted hazard ratio?=?3.35 [1.76 to 6.39]).<br>
Conclusions In cognitively normal individuals, A?+?T?+?compounds brain atrophy and cognitive deterioration, amplifying the likelihood of disease progression. Therapeutic interventions targeting A?+?T?+?individuals could be pivotal in curbing brain atrophy, cognitive decline, and disease progression.
en-copyright=
kn-copyright=

en-aut-name=FujishimaMotonobu
en-aut-sei=Fujishima
en-aut-mei=Motonobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawasakiYohei
en-aut-sei=Kawasaki
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MitsuhashiToshiharu
en-aut-sei=Mitsuhashi
en-aut-mei=Toshiharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MatsudaHiroshi
en-aut-sei=Matsuda
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Radiology, Kumagaya General Hospital
kn-affil=

affil-num=2
en-affil=Department of Biostatistics, Graduate School of Medicine, Saitama Medical University
kn-affil=

affil-num=3
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Biofunctional Imaging, Fukushima Medical University
kn-affil=
en-keyword=Preclinical
kn-keyword=Preclinical
en-keyword=Alzheimer�fs disease
kn-keyword=Alzheimer�fs disease
en-keyword=Longitudinal MRI
kn-keyword=Longitudinal MRI
en-keyword=Tau
kn-keyword=Tau
en-keyword=Amyloid-��
kn-keyword=Amyloid-��
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=4
article-no=
start-page=253
end-page=259
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202508
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Study of Periprosthetic Femoral Stem Fractures in Hip Arthroplasty for Femoral Neck Fracture
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the risk factors for bone fragility and perioperative periprosthetic femoral stem fractures in patients undergoing hip arthroplasty for femoral neck fractures. The records of 215 patients (42 male, 173 female; mean age, 84.4 years) were analyzed to assess correlations among periprosthetic fracture rates and sex, age, body mass index (BMI), Dorr classification, femoral stem fixation type (cemented/cementless), and bone mineral density (BMD) of the contralateral proximal femur. The overall prevalence of perioperative periprosthetic fractures was 4.7%. All patients with periprosthetic fractures were female, and all but one were ? 80 years of age. Fracture rates were higher in patients with lower BMI, although this difference was not significant. The fracture rates were 0%, 4.7%, and 7.9% for Dorr types A, B, and C, respectively, and 0% and 5.3% for patients who received cemented and cementless stems, respectively. The findings indicated that female patients, those of advanced age, those with lower BMI, and those with Dorr type C had lower BMDs. Although BMD was significantly lower in patients who received cemented stems compared to those who received cementless stems, no fractures were observed in the former group, suggesting that the use of cemented stems is safe for this high-risk population.
en-copyright=
kn-copyright=

en-aut-name=MiyakeYoshiaki
en-aut-sei=Miyake
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakagiToru
en-aut-sei=Takagi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KonishiikeTaizo
en-aut-sei=Konishiike
en-aut-mei=Taizo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=

affil-num=3
en-affil=Department of Orthopaedic Surgery, Japanese Red Cross Okayama Hospital
kn-affil=
en-keyword=bone mineral density
kn-keyword=bone mineral density
en-keyword=cemented stem
kn-keyword=cemented stem
en-keyword=Dorr classification
kn-keyword=Dorr classification
en-keyword=femoral neck fracture
kn-keyword=femoral neck fracture
en-keyword=periprosthetic femoral stem fracture
kn-keyword=periprosthetic femoral stem fracture
END

start-ver=1.4
cd-journal=joma
no-vol=31
cd-vols=
no-issue=
article-no=
start-page=100776
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Investigation of the relationship between 0.5?1200?Hz signal characteristics of cortical high-frequency oscillations and epileptogenicity through multivariate analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fast ripples (FRs) (250?500 Hz) on the electroencephalogram (EEG) are closely related to epileptogenicity and are important to determine cortical regions resected in epilepsy surgery. However, FR-related epileptogenicity may be variable, and may depend on information associated with FRs. We enrolled nine epilepsy patients who had undergone intracranial 5 kHz-sampling-rate EEG for surgical treatment and had final Engel class I outcomes. Three electrodes were selected from each epileptogenic area (EA) and the unlikely EA (the region outside the EA) in each patient. Up to 100 candidate FRs were automatically detected from interictal nocturnal EEG at each of the selected electrodes and were visually reviewed independently by two researchers. Multivariate logistic regression analysis was performed using the frequency and log-power value of the corresponding FRs, presence of concurrent spike, ripple, very-high-frequency oscillations (vHFO)1 (500?600 Hz), and vHFO2 (600?1200 Hz), and whether the timing of the spectral peak of corresponding FRs was in the peak?trough or trough?peak transition of each slow activity (0.5?1, 1?2, 2?3, 3?4, and 4?8 Hz) as independent variables. Factors significantly related to epileptogenicity were FR power, the concurrent presence of spike and vHFO2, coupling with 0.5?1 and 1?2 Hz slow waves in the peak?trough transition, and coupling with 3?4 and 4?8 Hz slow waves in the trough?peak transition. Multifactorial analysis of FRs may increase their usefulness, potentially leading to improved treatment outcomes in epilepsy surgery.
en-copyright=
kn-copyright=

en-aut-name=ShibataTakashi
en-aut-sei=Shibata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsuchiyaHiroki
en-aut-sei=Tsuchiya
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AkiyamaMari
en-aut-sei=Akiyama
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkiyamaTomoyuki
en-aut-sei=Akiyama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsuhashiMasao
en-aut-sei=Matsuhashi
en-aut-mei=Masao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Epilepsy, Movement Disorders and Physiology, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=6
en-affil=Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital
kn-affil=
en-keyword=Epilepsy surgery
kn-keyword=Epilepsy surgery
en-keyword=Multivariate logistic regression analysis
kn-keyword=Multivariate logistic regression analysis
en-keyword=Phase-amplitude coupling
kn-keyword=Phase-amplitude coupling
en-keyword=Ripple
kn-keyword=Ripple
en-keyword=Very high-frequency oscillations
kn-keyword=Very high-frequency oscillations
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=1
article-no=
start-page=104318
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hypotheses of pathophysiological mechanisms in epileptic encephalopathies: A review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: Epileptic encephalopathy (EE) is a serious clinical issue that manifests as part of developmental and epileptic encephalopathy (DEE), particularly in childhood epilepsy. In EE, neurocognitive functions and behavior are impaired by intense epileptiform electroencephalogram (EEG) activity. Hypotheses of pathophysiological mechanisms behind EE are reviewed to contribute to an effective solution for EE.<br>
Review: Current hypotheses are as follows: 1) neuronal dysfunction based on genetic abnormalities that may affect neurocognitive functions and epilepsy separately; 2) impairment of synaptic homeostasis during sleep that may be responsible for DEE/EE with spike-and-wave activation in sleep; 3) abnormal subcortical regulation of the cerebral cortex; 4) abnormal cortical metabolism and hemodynamics with impairment of the neural network including default mode network; 5) neurotransmitter imbalance and disordered neural excitability; 6) the effects of neuroinflammation that may be caused by epileptic seizures and in turn aggravate epileptogenesis; 7) the interaction between physiological and pathological high-frequency EEG activity; etc. The causal relationship between epileptiform EEG activity and neurocognitive dysfunctions is small in DEE based on genetic abnormalities and it is largely unestablished in the other hypothetical mechanisms.<br>
Conclusion: We have not yet found answers to the question of whether the single-central or multiple derangements are present and what seizures and intense epileptiform EEG abnormalities mean in EE. We need to continue our best efforts in both aspects to elucidate the pathophysiological mechanisms of DEE/EE and further develop epilepsy treatment and precision medicine.
en-copyright=
kn-copyright=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShibataTakashi
en-aut-sei=Shibata
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsuchiyaHiroki
en-aut-sei=Tsuchiya
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkiyamaMari
en-aut-sei=Akiyama
en-aut-mei=Mari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=AkiyamaTomoyuki
en-aut-sei=Akiyama
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Pediatrics, Asahigawaso Rehabilitation and Medical Center
kn-affil=

affil-num=2
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pediatric Neurology, Okayama University Hospital and Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Behavior
kn-keyword=Behavior
en-keyword=Childhood epilepsy
kn-keyword=Childhood epilepsy
en-keyword=Cognitive function
kn-keyword=Cognitive function
en-keyword=Developmental and epileptic encephalopathy
kn-keyword=Developmental and epileptic encephalopathy
en-keyword=Regression
kn-keyword=Regression
END

start-ver=1.4
cd-journal=joma
no-vol=272
cd-vols=
no-issue=1
article-no=
start-page=36
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genetic and functional analyses of SPTLC1 in juvenile amyotrophic lateral sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder of the motor system. Pathogenic variants in SPTLC1, encoding a subunit of serine palmitoyltransferase, cause hereditary sensory and autonomic neuropathy type 1 (HSAN1), and have recently been associated with juvenile ALS. SPTLC1 variants associated with ALS cause elevated levels of sphinganines and ceramides. Reports on ALS associated with SPTLC1 remain limited. This study aimed to investigate the frequency of SPTLC1 variants in ALS and relevant clinical characteristics.<br>
Methods We analyzed whole-exome and whole-genome sequence data from 40 probands with familial ALS and 413 patients with sporadic ALS without previously identified causative variants. Reverse transcription polymerase chain reaction (RT-PCR) analysis and droplet digital PCR (ddPCR) were used to assess splicing and mosaicism, respectively. Plasma sphingolipid levels were quantified to analyze biochemical consequences.<br>
Results The heterozygous c.58G>A, p.Ala20Thr variant was identified in a 21-year-old Japanese female patient presenting with symmetric weakness which slowly progressed over 15 years. RT-PCR analysis showed no splice defects. Plasma sphingolipid levels in the patient were significantly increased compared to her asymptomatic parents. ddPCR revealed that the asymptomatic father harbored a mosaic variant with 17% relative mutant allele abundance in peripheral blood leukocytes.<br>
Conclusions We identified a pathogenic c.58G>A, p.Ala20Thr SPTLC1 variant in a patient with juvenile ALS, likely inherited from an asymptomatic parent with mosaicism. Lipid analysis results are consistent with previous findings on SPTLC1-associated ALS. Further studies are necessary to determine the clinical effect of mosaic variants of SPTLC1.
en-copyright=
kn-copyright=

en-aut-name=OkuboSo
en-aut-sei=Okubo
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaruseHiroya
en-aut-sei=Naruse
en-aut-mei=Hiroya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SudoAtsushi
en-aut-sei=Sudo
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=EsakiKayoko
en-aut-sei=Esaki
en-aut-mei=Kayoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SatakeWataru
en-aut-sei=Satake
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=GreimelPeter
en-aut-sei=Greimel
en-aut-mei=Peter
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ShingaiNanoka
en-aut-sei=Shingai
en-aut-mei=Nanoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OyaYasushi
en-aut-sei=Oya
en-aut-mei=Yasushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YoshikawaTakeo
en-aut-sei=Yoshikawa
en-aut-mei=Takeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=5
en-affil=Department of Biotechnology and Life Sciences, Faculty of Biotechnology and Life Sciences, Sojo University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Laboratory for Cell Function Dynamics, RIKEN Centre for Brain Sciences
kn-affil=

affil-num=10
en-affil=Division of Applied Life Science, Graduate School of Engineering, Sojo University
kn-affil=

affil-num=11
en-affil=Department of Neurology, National Center of Neurology and Psychiatry
kn-affil=

affil-num=12
en-affil=Laboratory of Molecular Psychiatry, RIKEN Center for Brain Science
kn-affil=

affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=Juvenile amyotrophic lateral sclerosis
kn-keyword=Juvenile amyotrophic lateral sclerosis
en-keyword=SPTLC1
kn-keyword=SPTLC1
en-keyword=Sphingolipids
kn-keyword=Sphingolipids
en-keyword=Mosaicism
kn-keyword=Mosaicism
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=12
article-no=
start-page=1900
end-page=1905
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250615
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Subacute Upper Motor Neuron Dysfunction Possibly Associated with the Anti-GM1 Autoantibody
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anti-GM1 antibodies are associated with Guillain-Barr? syndrome (GBS), primarily peripheral neuropathy. However, there are cases of anti-GM1 IgG antibody-positive GBS with upper motor neuron (UMN) signs. We herein report a case of gastrointestinal infection followed by subacute gait disturbance with predominant signs of UMN on a neurological examination. The serum and cerebrospinal fluid tests were positive for anti-GM1 and anti-asialo-GM1 IgG antibodies. An electrophysiological evaluation revealed normal nerve conduction and prolonged central motor conduction times. No magnetic resonance imaging abnormalities were observed. The symptoms improved with treatment, which was accompanied by decreased antibody titers. This case highlights the fact that anti-GM1 IgG-associated disorders may present with predominant UMN involvement.
en-copyright=
kn-copyright=

en-aut-name=OkuboSo
en-aut-sei=Okubo
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MaedaMeiko
en-aut-sei=Maeda
en-aut-mei=Meiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatsuseKazuto
en-aut-sei=Katsuse
en-aut-mei=Kazuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShirotaYuichiro
en-aut-sei=Shirota
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HamadaMasashi
en-aut-sei=Hamada
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatakeWataru
en-aut-sei=Satake
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=anti-GM1 antibody
kn-keyword=anti-GM1 antibody
en-keyword=anti-GA1 antibody
kn-keyword=anti-GA1 antibody
en-keyword=upper motor neuron
kn-keyword=upper motor neuron
en-keyword=motor-evoked potentials
kn-keyword=motor-evoked potentials
en-keyword=central motor conduction time
kn-keyword=central motor conduction time
en-keyword=Guillain-Barr? syndrome
kn-keyword=Guillain-Barr? syndrome
END

start-ver=1.4
cd-journal=joma
no-vol=638
cd-vols=
no-issue=8049
article-no=
start-page=225
end-page=236
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Immune evasion through mitochondrial transfer in the tumour microenvironment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cancer cells in the tumour microenvironment use various mechanisms to evade the immune system, particularly T?cell attack1. For example, metabolic reprogramming in the tumour microenvironment and mitochondrial dysfunction in tumour-infiltrating lymphocytes (TILs) impair antitumour immune responses2,3,4. However, detailed mechanisms of such processes remain unclear. Here we analyse clinical specimens and identify mitochondrial DNA (mtDNA) mutations in TILs that are shared with cancer cells. Moreover, mitochondria with mtDNA mutations from cancer cells are able to transfer to TILs. Typically, mitochondria in TILs readily undergo mitophagy through reactive oxygen species. However, mitochondria transferred from cancer cells do not undergo mitophagy, which we find is due to mitophagy-inhibitory molecules. These molecules attach to mitochondria and together are transferred to TILs, which results in homoplasmic replacement. T?cells that acquire mtDNA mutations from cancer cells exhibit metabolic abnormalities and senescence, with defects in effector functions and memory formation. This in turn leads to impaired antitumour immunity both in vitro and in vivo. Accordingly, the presence of an mtDNA mutation in tumour tissue is a poor prognostic factor for immune checkpoint inhibitors in patients with melanoma or non-small-cell lung cancer. These findings reveal a previously unknown mechanism of cancer immune evasion through mitochondrial transfer and can contribute to the development of future cancer immunotherapies.
en-copyright=
kn-copyright=

en-aut-name=IkedaHideki
en-aut-sei=Ikeda
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaseKatsushige
en-aut-sei=Kawase
en-aut-mei=Katsushige
kn-aut-name=
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en-aut-name=KawazuMasahito
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affil-num=1
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=2
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=3
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Division of Innovative Cancer Therapeutics, Chiba Cancer Center Research Institute
kn-affil=

affil-num=6
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=7
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Division of Nutriomics and Oncology, RCAST, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
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affil-num=10
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute, Chiba, Japan Department of Dermatology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=11
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

affil-num=14
en-affil=Tsuruoka Metabolomics Laboratory, National Cancer Center
kn-affil=

affil-num=15
en-affil=Department of Surgical Pathology, Chiba Cancer Center
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affil-num=16
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=17
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=18
en-affil=Laboratory of Evolutionary Oncology, Chiba Cancer Center Research Institute
kn-affil=

affil-num=19
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=20
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=21
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=22
en-affil=Department of Dermatology, Faculty of Medicine, University of Yamanashi
kn-affil=

affil-num=23
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=24
en-affil=Department of Skin Oncology/Dermatology, Saitama Medical University International Medical Center
kn-affil=

affil-num=25
en-affil=Department of Dermatology, Shinshu University School of Medicine
kn-affil=

affil-num=26
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=27
en-affil=Department of Medical Oncology, Kindai University Faculty of Medicine
kn-affil=

affil-num=28
en-affil=Department of Diagnostic Pathology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=29
en-affil=Department of Otorhinolaryngology/Head and Neck Surgery, Chiba University Graduate School of Medicine
kn-affil=

affil-num=30
en-affil=Department of General Thoracic Surgery and Endocrinological Surgery, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=31
en-affil=Division of Cellular Signalling, National Cancer Center Research Institute
kn-affil=

affil-num=32
en-affil=Department of Respirology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=33
en-affil=Division of Nutriomics and Oncology, RCAST, The University of Tokyo
kn-affil=

affil-num=34
en-affil=Division of Cell Therapy, Chiba Cancer Center Research Institute
kn-affil=

affil-num=35
en-affil=Department of Tumor Microenvironment, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=5
article-no=
start-page=271
end-page=277
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240329
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Japan MSA registry: A multicenter cohort study of multiple system atrophy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by autonomic failure and various motor symptoms. While MSA-C (cerebellar type) predominates in East Asia, MSA-P (parkinsonian type) predominates in Europe and North America. This nationwide patient registry aimed to (1) conduct a prospective natural history study of MSA in Japan, (2) facilitate patient recruitment for clinical trials, and (3) deposit bioresources and clinical information in a biobank.<br>
Methods: Thirteen institutions participated in this study. Clinical information was obtained by neurologists from the patients visiting the hospital every 12?months to assess the UMSARS Part 2 scores and by telephone interviews by nurses every 6?months to assess UMSARS Part 1 scores and to determine whether clinical events had occurred.<br>
Results: Demographic data from 329 MSA patients (216 MSA-C and 113 MSA-P) were analyzed. The mean age at symptom onset was 58.2?years (standard deviation, 8.9); the mean duration of symptoms at enrollment was 3.5?years (standard deviation, 2.2). The mean 12-month changes in the UMSARS Part 1 and Part 2 scores were 7.9 (standard deviation, 5.6) and 6.4 (standard deviation, 5.9), respectively. The patient registry proved useful in recruiting participants for clinical trials, including those with gene variants. Clinical information and biospecimens were deposited in a biobank.<br>
Discussion: The study highlighted the importance of telephone interviews in minimizing drop-out rates in natural history studies and demonstrated similar MSA progression rates across populations. The deposited bioresources are available to researchers upon request, aiming to contribute to future MSA researches.
en-copyright=
kn-copyright=

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affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
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kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
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affil-num=5
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affil-num=6
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affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
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affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
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affil-num=9
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Neurology, Nagoya University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=13
en-affil=Department of Neurology, Brain Research Institute, Niigata University
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=16
en-affil=Department of Neurology, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=17
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=18
en-affil=Department of Human Health Sciences, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=19
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=20
en-affil=Department of Neurology, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=21
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=22
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=23
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=24
en-affil=Division of Neurology, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University
kn-affil=

affil-num=25
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=26
en-affil=Department of Neurology, Okayama University Graduate School of Medicine and Dentistry
kn-affil=

affil-num=27
en-affil=Department of Neurology and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=

affil-num=28
en-affil=Department of Neurology and Geriatrics, Graduate School of Medical and Dental Sciences, Kagoshima University
kn-affil=

affil-num=29
en-affil=Department of Neurology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=30
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=31
en-affil=Department of Neurology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University
kn-affil=

affil-num=32
en-affil=Department of Neurology, Higashi-Saitama National Hospital
kn-affil=

affil-num=33
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=34
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=35
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=36
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=37
en-affil=Department of Neurology and Neurological Science, Tokyo Medical and Dental University
kn-affil=

affil-num=38
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=multicenter cohort study
kn-keyword=multicenter cohort study
en-keyword=multiple system atrophy
kn-keyword=multiple system atrophy
en-keyword=natural history
kn-keyword=natural history
en-keyword=patient registry
kn-keyword=patient registry
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=10
article-no=
start-page=1215
end-page=1227
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241121
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Enhanced design of pCMViR-TSC plasmid vector for sustainably high cargo gene expression in mammalian cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The first-generation pCMViR-TSC, implemented through the promoter sandwich rule, yields 10- to 100-fold higher gene expression than the standard plasmid used with the CMV (cytomegalovirus) or CAG promoter. However, the vector�fs shortcomings limit its utility to transient expression only, as it is not suitable for establishing stable transformants in mammalian cells. To overcome this weakness, we here introduce the improved plasmid vector pSAKA-4B, derived from pCMViR-TSC as a second-generation chromosome-insertable vector. This vector facilitates the linear entry of the expression unit into the TTAA site of DNA universally with transposase assistance. The vector is helpful for the indefinite expression of our target gene. The new vector system is proven here to be efficient in establishing stable transformants with a high likelihood of positive clones that exhibit significantly elevated expression levels of the delivered foreign gene. This system, alongside the first-generation vector, is therefore instrumental for diverse basic research endeavors concerning genes, proteins, cells, and animals, and potentially for clinical applications such as gene therapy.
en-copyright=
kn-copyright=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakaguchiYoshihiko
en-aut-sei=Sakaguchi
en-aut-mei=Yoshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FutamiJunichiro
en-aut-sei=Futami
en-aut-mei=Junichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamauchiAkira
en-aut-sei=Yamauchi
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakahashiTetta
en-aut-sei=Takahashi
en-aut-mei=Tetta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=GoharaYuma
en-aut-sei=Gohara
en-aut-mei=Yuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=JiangFan
en-aut-sei=Jiang
en-aut-mei=Fan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KomalasariNi Luh Gede Yoni
en-aut-sei=Komalasari
en-aut-mei=Ni Luh Gede Yoni
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=ChenYouyi
en-aut-sei=Chen
en-aut-mei=Youyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=RumaI Made Winarsa
en-aut-sei=Ruma
en-aut-mei=I Made Winarsa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=SumardikaI Wayan
en-aut-sei=Sumardika
en-aut-mei=I Wayan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=ZhouJin
en-aut-sei=Zhou
en-aut-mei=Jin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=HonjoTomoko
en-aut-sei=Honjo
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=KuribayashiFutoshi
en-aut-sei=Kuribayashi
en-aut-mei=Futoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SagayamaKazumi
en-aut-sei=Sagayama
en-aut-mei=Kazumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=KondoEisaku
en-aut-sei=Kondo
en-aut-mei=Eisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=InoueYusuke
en-aut-sei=Inoue
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Microbiology, Tokushima Bunri University
kn-affil=

affil-num=5
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=12
en-affil=Department of Cell Biology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=13
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=14
en-affil=Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
kn-affil=

affil-num=15
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=16
en-affil=Faculty of Medicine, Udayana University
kn-affil=

affil-num=17
en-affil=Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
kn-affil=

affil-num=18
en-affil=Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=19
en-affil=Department of Biochemistry, Kawasaki Medical School
kn-affil=

affil-num=20
en-affil=Organization for Research and Innovation Strategy, Okayama University
kn-affil=

affil-num=21
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=22
en-affil=Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
kn-affil=

affil-num=23
en-affil=Faculty of Science and Technology, Division of Molecular Science, Gunma University
kn-affil=
en-keyword=Plasmid
kn-keyword=Plasmid
en-keyword=Gene engineering
kn-keyword=Gene engineering
en-keyword=Cancer
kn-keyword=Cancer
en-keyword=Cell culture
kn-keyword=Cell culture
END

start-ver=1.4
cd-journal=joma
no-vol=150
cd-vols=
no-issue=1
article-no=
start-page=19
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Biallelic variants in DNAJC7 cause familial amyotrophic lateral sclerosis with the TDP-43 pathology
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive degeneration of motor neurons. ALS pathology primarily involves the failure of protein quality control mechanisms, leading to the accumulation of misfolded proteins, particularly TAR DNA-binding protein 43 (TDP-43). TDP-43 aggregation is a central pathological feature of ALS. Maintaining protein homeostasis is critical and facilitated by heat shock proteins (HSPs), particularly the HSP40 family, which includes co-chaperones such as DNAJC7. Here, we report a family with three siblings affected by ALS who carry a homozygous c.518dupC frameshift variant in DNAJC7, a member of the HSP40 family. All three patients exhibited progressive muscle weakness, limb atrophy, bulbar palsy, and respiratory failure. Pathological examination revealed degeneration of both upper and lower motor neurons, with phosphorylated TDP-43-positive neuronal cytoplasmic inclusions in the frontal and temporal cortices. Immunoblot analysis were consistent with a type B pattern of phosphorylated TDP-43 in the precentral gyrus. Immunohistochemistry and RNA sequencing analyses demonstrated a substantial reduction in DNAJC7 expression at both the protein and RNA levels in affected brain regions. In a TDP-43 cell model, DNAJC7 knockdown impaired the disassembly of TDP-43 following arsenite-induced stress, whereas DNAJC7 overexpression suppressed the assembly and promoted the disassembly of arsenite-induced TDP-43 condensates. Furthermore, in a zebrafish ALS model, dnajc7 knockdown resulted in increased TDP-43 aggregation in motor neurons and reduced survival. To the best of our knowledge, this study provides the first evidence linking biallelic loss-of-function variants in DNAJC7 to familial ALS with TDP-43 pathology.
en-copyright=
kn-copyright=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OusakaDaiki
en-aut-sei=Ousaka
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Ota-ElliottRicardo Satoshi
en-aut-sei=Ota-Elliott
en-aut-mei=Ricardo Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KawanoTomohito
en-aut-sei=Kawano
en-aut-mei=Tomohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HosonoYasuyuki
en-aut-sei=Hosono
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurology, National Hospital Organisation Minami-Okayama Medical Centre
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Psychiatry, Zikei Hospital
kn-affil=

affil-num=10
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Brain and Neurosciences, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=14
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Amyotrophic lateral sclerosis
kn-keyword=Amyotrophic lateral sclerosis
en-keyword=Heat shock protein
kn-keyword=Heat shock protein
en-keyword=DNAJC7
kn-keyword=DNAJC7
en-keyword=TDP-43
kn-keyword=TDP-43
en-keyword=Live-cell imaging
kn-keyword=Live-cell imaging
en-keyword=Zebrafish disease model
kn-keyword=Zebrafish disease model
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=6
article-no=
start-page=e00110-25
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250519
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mycobacterium tuberculosis bacillus induces pyroptosis in human lung fibroblasts
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We previously reported that live, but not dead, virulent Mycobacterium tuberculosis (Mtb) H37Rv bacilli induce cell death in human lung fibroblast cell lines, MRC-5, MRC-9, and TIG-1. Here, using two distinct Mtb strains from two different lineages (HN878 lineage 2 and H37Rv lineage 4), we confirmed cell death at day 2 after infection with a device that measures cell growth/cytotoxicity in real time (Maestro-Z [AXION]). Mtb bacilli uptake by the fibroblast was confirmed with a transmission electron microscope on day 2. Expressions of inflammatory cytokines and interleukin (IL)?1��, IL-6, and IL-8 were observed when exposed to live, but not dead bacteria. The cell death of fibroblasts induced by both Mtb strains tested was prevented by caspase-1/4 and NLRP3 inflammasome inhibitors, but not by caspase-3 and caspase-9 inhibitors. Therefore, we classified the fibroblast cell death by Mtb infection as pyroptosis. To investigate the biological and pathological relevance of fibroblast cell death by Mtb infection, we performed dual RNA-Seq analysis on Mtb within fibroblasts and Mtb-infected fibroblasts at day 2. In Mtb bacilli tcrR, secE2, ahpD, and mazF8 genes were highly induced during infection. These genes play roles in survival in a hypoxic environment, production of a calcium-binding protein-inducing cytokine, and regulation of transcription in a toxin-antitoxin system. The gene expressions of IL-1��, IL-6, and IL-8, caspase-4, and NLRP3, but not of caspase-3 and caspase-9, were augmented in Mtb bacilli-infected fibroblasts. Taken together, our study suggests that Mtb bacilli attempt to survive in lung fibroblasts and that pyroptosis of the host fibroblasts activates the immune system against the infection.
en-copyright=
kn-copyright=

en-aut-name=TakiiTakemasa
en-aut-sei=Takii
en-aut-mei=Takemasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaHiroyuki
en-aut-sei=Yamada
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotozonoChihiro
en-aut-sei=Motozono
en-aut-mei=Chihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamasakiSho
en-aut-sei=Yamasaki
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TorrellesJordi B.
en-aut-sei=Torrelles
en-aut-mei=Jordi B.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TurnerJoanne
en-aut-sei=Turner
en-aut-mei=Joanne
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimishimaAoi
en-aut-sei=Kimishima
en-aut-mei=Aoi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsamiYukihiro
en-aut-sei=Asami
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OharaNaoya
en-aut-sei=Ohara
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HidaShigeaki
en-aut-sei=Hida
en-aut-mei=Shigeaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HayashiHidetoshi
en-aut-sei=Hayashi
en-aut-mei=Hidetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OnozakiKikuo
en-aut-sei=Onozaki
en-aut-mei=Kikuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Mycobacterium Reference and Research, the Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association
kn-affil=

affil-num=2
en-affil=Department of Mycobacterium Reference and Research, the Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association
kn-affil=

affil-num=3
en-affil=Department of Molecular Immunology, Research Institute for Microbial Diseases, The University of Osaka
kn-affil=

affil-num=4
en-affil=Department of Molecular Immunology, Research Institute for Microbial Diseases, The University of Osaka
kn-affil=

affil-num=5
en-affil=Texas Biomedical Research Institute and International Center for the Advancement of Research & Education (I?CARE)
kn-affil=

affil-num=6
en-affil=Texas Biomedical Research Institute and International Center for the Advancement of Research & Education (I?CARE)
kn-affil=

affil-num=7
en-affil=Laboratory of Applied Microbial Chemistry, ?mura Satoshi Memorial Institute, Kitasato University
kn-affil=

affil-num=8
en-affil=Laboratory of Applied Microbial Chemistry, ?mura Satoshi Memorial Institute, Kitasato University
kn-affil=

affil-num=9
en-affil=Department of Oral Microbiology, Graduate School of Medicine, Density and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Hygienic Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=

affil-num=11
en-affil=Department of Cell Signaling, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=

affil-num=12
en-affil=Department of Hygienic Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University
kn-affil=
en-keyword=Mycobacterium tuberculosis
kn-keyword=Mycobacterium tuberculosis
en-keyword=pyroptosis
kn-keyword=pyroptosis
en-keyword=caspase
kn-keyword=caspase
en-keyword=RNA-Seq
kn-keyword=RNA-Seq
en-keyword=cytokine
kn-keyword=cytokine
en-keyword=fibroblasts
kn-keyword=fibroblasts
END

start-ver=1.4
cd-journal=joma
no-vol=33
cd-vols=
no-issue=3
article-no=
start-page=99
end-page=117
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240429
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Generation and characterization of cerebellar granule neurons specific knockout mice of Golli-MBP
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Golli?myelin basic proteins, encoded by the myelin basic protein gene, are widely expressed in neurons and oligodendrocytes in the central nervous system. Further, prior research has shown that Golli?myelin basic protein is necessary for myelination and neuronal maturation during central nervous system development. In this study, we established Golli?myelin basic protein-floxed mice to elucidate the cell-type-specific effects of Golli?myelin basic protein knockout through the generation of conditional knockout mice (Golli?myelin basic proteinsfl/fl; E3CreN), in which Golli?myelin basic proteins were specifically deleted in cerebellar granule neurons, where Golli?myelin basic proteins are expressed abundantly in wild-type mice. To investigate the role of Golli?myelin basic proteins in cerebellar granule neurons, we further performed histopathological analyses of these mice, with results indicating no morphological changes or degeneration of the major cellular components of the cerebellum. Furthermore, behavioral analysis showed that Golli?myelin basic proteinsfl/fl; E3CreN mice were healthy and did not display any abnormal behavior. These results suggest that the loss of Golli?myelin basic proteins in cerebellar granule neurons does not lead to cerebellar perturbations or behavioral abnormalities. This mouse model could therefore be employed to analyze the effect of Golli?myelin basic protein deletion in specific cell types of the central nervous system, such as other neuronal cells and oligodendrocytes, or in lymphocytes of the immune system.
en-copyright=
kn-copyright=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishiokaSaki
en-aut-sei=Nishioka
en-aut-mei=Saki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamanakaTomoyuki
en-aut-sei=Yamanaka
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeManabu
en-aut-sei=Abe
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ImamuraYukio
en-aut-sei=Imamura
en-aut-mei=Yukio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyasakaTomohiro
en-aut-sei=Miyasaka
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KakudaNobuto
en-aut-sei=Kakuda
en-aut-mei=Nobuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShimogoriTomomi
en-aut-sei=Shimogori
en-aut-mei=Tomomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamakawaKazuhiro
en-aut-sei=Yamakawa
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IkawaMasahito
en-aut-sei=Ikawa
en-aut-mei=Masahito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=NukinaNobuyuki
en-aut-sei=Nukina
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=2
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=3
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=4
en-affil=Department of Animal Model Development, Brain Research Institute, Niigata University
kn-affil=

affil-num=5
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=

affil-num=6
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

affil-num=7
en-affil=Faculty of Life and Medical Sciences, Doshisha University
kn-affil=

affil-num=8
en-affil=Department of Molecular Biology and Biochemistry, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Laboratory for Molecular Mechanisms of Brain Development, RIKEN Center for Brain Science
kn-affil=

affil-num=10
en-affil=Laboratory for Neurogenetics, RIKEN Center for Brain Science
kn-affil=

affil-num=11
en-affil=Department of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University
kn-affil=

affil-num=12
en-affil=Laboratory of Structural Neuropathology, Graduate School of Brain Science, Doshisha University
kn-affil=
en-keyword=Golli-MBP
kn-keyword=Golli-MBP
en-keyword=Cerebellar granule neuron
kn-keyword=Cerebellar granule neuron
en-keyword=CRISPR/Cas9
kn-keyword=CRISPR/Cas9
en-keyword=Conditional knockout
kn-keyword=Conditional knockout
END

start-ver=1.4
cd-journal=joma
no-vol=218
cd-vols=
no-issue=
article-no=
start-page=104922
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Alteration of perineuronal nets and parvalbumin interneurons in prefrontal cortex and hippocampus, and correlation with blood corticosterone in activity-based anorexia model mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anorexia nervosa (AN) is an eating disorder characterized by restricted energy intake, severely underweight status, and frequent hyperactivity. Previous research has shown structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus of AN patients. To investigate the pathological mechanism of AN, we analyzed the expression and distribution of parvalbumin (PV) interneurons and perineuronal nets (PNNs), which are implicated in the pathology of neuropsychiatric disorders, in the mPFC and hippocampus dorsal (HPCd) and ventral (HPCv) using an activity-based anorexia (ABA) mouse model. We found that PNN expression and density increased in the mPFC, with minor alterations in the HPCd and HPCv of ABA mice. The expression and distribution of PV neurons were unchanged in the brains of ABA mice, except for a regional decrease in PV-expressing neuron density in the HPCd. Co-localization analysis showed an increased number of PNNs enwrapping PV-negative neurons in the mPFC of ABA mice. Furthermore, the upregulation of PNN expression in the mPFC was positively correlated with elevated blood corticosterone levels, a well-known stress indicator, in ABA mice. Our findings suggest that the increased expression and distribution of PNNs surrounding PV-negative neurons in the mPFC may indicate the pathological mechanisms of AN.
en-copyright=
kn-copyright=

en-aut-name=NguyenHoang Duy
en-aut-sei=Nguyen
en-aut-mei=Hoang Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiHaruko
en-aut-sei=Miyazaki
en-aut-mei=Haruko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaiHiroki
en-aut-sei=Kawai
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WangZiyi
en-aut-sei=Wang
en-aut-mei=Ziyi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakamotoShinji
en-aut-sei=Sakamoto
en-aut-mei=Shinji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OohashiToshitaka
en-aut-sei=Oohashi
en-aut-mei=Toshitaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neuropsychiatry, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=anorexia nervosa
kn-keyword=anorexia nervosa
en-keyword=activity-based anorexia
kn-keyword=activity-based anorexia
en-keyword=perineuronal nets
kn-keyword=perineuronal nets
en-keyword=parvalbumin
kn-keyword=parvalbumin
en-keyword=corticosterone
kn-keyword=corticosterone
en-keyword=prefrontal cortex
kn-keyword=prefrontal cortex
en-keyword=hippocampus
kn-keyword=hippocampus
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=9
article-no=
start-page=e70105
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250724
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ultrahigh�]Field MR�]Compatible Mechanical Tactile Stimulator for Investigating Somatosensory Processing in Small�]Bodied Animals
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Common marmosets (Callithrix jacchus), small-bodied New World primates that share similar sensory processing pathways with human beings, have gained great interests. Their small body size allows imaging of brain activity with high spatial resolution and on a whole-brain scale using ultrahigh-field (UHF) magnetic resonance imaging (MRI) scanners. However, the strong magnetic field and the small size of the hand and forearm pose challenges in delivering tactile stimulation during fMRI experiments. In the present study, we developed an MR-compatible tactile dual-point stimulator to provide high-precision mechanical stimulation for exploring somatosensory processing in small-bodied animals. The study population consisted of a water phantom and three male common marmosets. Cerebral blood volume (CBV) weighted fMRI data were obtained with a gradient echo (GE), echo-planar imaging (EPI) sequence at 7T scanner. The output performance of the device was tested by a pressure sensor. The MR compatibility of the device was verified by measuring the temporal signal-to-noise ratio (tSNR) of a water phantom. To test the effectiveness of tactile stimulation, we conducted block designed tactile stimulation experiments on marmosets. A one-way repeated measures ANOVA was conducted for comparing the tSNR results. We performed one-sample t-tests to investigate the negative response of the forearm and hand stimulation with a threshold of t > 1.96 (p < 0.05). Performance tests revealed that mechanical stimulation (averaged force: 31.69?g) was applied with a delay of 12?ms. Phantom experiments confirmed that there was no significant difference in the tSNR among three (10?Hz, 1?Hz, and no-stimulus) conditions (F (2, 798) = 0.71, p = 0.49). The CBV activity results showed that the stimulator successfully elicited hand and forearm somatosensory activations in primary somatosensory areas. These results indicated that the device is well suited for small-bodied animal somatosensory studies.
en-copyright=
kn-copyright=

en-aut-name=WangChenyu
en-aut-sei=Wang
en-aut-mei=Chenyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ImaiHirohiko
en-aut-sei=Imai
en-aut-mei=Hirohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukunagaMasaki
en-aut-sei=Fukunaga
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamamotoHiroki
en-aut-sei=Yamamoto
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SekiKazuhiko
en-aut-sei=Seki
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HanakawaTakashi
en-aut-sei=Hanakawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UmedaTatsuya
en-aut-sei=Umeda
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Innovation Research Center for Quantum Medicine, Gifu University School of Medicine
kn-affil=

affil-num=3
en-affil=Section of Brain Function Information, National Institute for Physiological Sciences
kn-affil=

affil-num=4
en-affil=Graduate School of Human and Environmental Studies, Kyoto University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurophysiology, National Center of Neurology and Psychiatry
kn-affil=

affil-num=7
en-affil=Department of Integrated Neuroanatomy and Neuroimaging, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=8
en-affil=Department of Integrated Neuroanatomy and Neuroimaging, Kyoto University Graduate School of Medicine
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=primary somatosensory cortex
kn-keyword=primary somatosensory cortex
en-keyword=small-bodied animals
kn-keyword=small-bodied animals
en-keyword=tactile stimulation device
kn-keyword=tactile stimulation device
en-keyword=ultrahigh-field magnetic resonance imaging
kn-keyword=ultrahigh-field magnetic resonance imaging
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=5
article-no=
start-page=594
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Review Article: Diagnostic Paradigm Shift in Spine Surgery
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Meticulous clinical examination is essential for spinal disorders to utilize the diagnostic methods and technologies that strongly support physicians and enhance clinical practice. A significant change in the approach to diagnosing spinal disorders has occurred in the last three decades, which has enhanced a more nuanced understanding of spine pathology. Traditional radiographic methods such as conventional and functional X-rays and CT scans are still the first line in the diagnosis of spinal disorders due to their low cost and accessibility. As more advanced imaging technologies become increasingly available worldwide, there is a constantly increasing trend in MRI scans for detecting spinal pathologies and making treatment decisions. Not only do MRI scans have superior diagnostic capabilities, but they also assist surgeons in performing meticulous preoperative planning, making them currently the most widely used diagnostic tool for spinal disorders. Positron Emission Tomography (PET) can help detect inflammatory lesions, infections, and tumors. Other advanced diagnostic tools such as CT/MRI fusion image, Functional Magnetic Resonance Imaging (fMRI), Upright and Kinetic MRI, magnetic resonance spectroscopy (MRS), diffusion-weighted imaging (DWI), and diffusion tensor imaging (DTI) could play an important role when it comes to detecting more special pathologies. However, some technical difficulties in the daily praxis and their high costs act as obstacles to their further spread. Integrating artificial intelligence and advancements in data analytics and virtual reality promises to enhance spinal procedures�f precision, safety, and efficacy. As these technologies continue to develop, they will play a critical role in transforming spinal surgery. This paradigm shift emphasizes the importance of continuous innovation and adaptability in improving the diagnosis and treatment of spinal disorders.
en-copyright=
kn-copyright=

en-aut-name=LeventAras Efe
en-aut-sei=Levent
en-aut-mei=Aras Efe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaMasato
en-aut-sei=Tanaka
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KumawatChetan
en-aut-sei=Kumawat
en-aut-mei=Chetan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HengChristian
en-aut-sei=Heng
en-aut-mei=Christian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NikolaosSalamalikis
en-aut-sei=Nikolaos
en-aut-mei=Salamalikis
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=LatkaKajetan
en-aut-sei=Latka
en-aut-mei=Kajetan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyamotoAkiyoshi
en-aut-sei=Miyamoto
en-aut-mei=Akiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KomatsubaraTadashi
en-aut-sei=Komatsubara
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AratakiShinya
en-aut-sei=Arataki
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OdaYoshiaki
en-aut-sei=Oda
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=ShinoharaKensuke
en-aut-sei=Shinohara
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UotaniKoji
en-aut-sei=Uotani
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=2
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=3
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=4
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=5
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=6
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=7
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=8
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=9
en-affil=Department of Orthopedic Surgery, Okayama Rosai Hospital
kn-affil=

affil-num=10
en-affil=Department of Orthopedic Surgery, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Orthopedic Surgery, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Orthopedic Surgery, Okayama University Hospital
kn-affil=
en-keyword=diagnosis
kn-keyword=diagnosis
en-keyword=spine surgery
kn-keyword=spine surgery
en-keyword=innovative technique
kn-keyword=innovative technique
en-keyword=MRI
kn-keyword=MRI
en-keyword=myelography
kn-keyword=myelography
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=12
article-no=
start-page=2429
end-page=2437
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241112
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Discovery of a Compound That Inhibits IRE1�� S-Nitrosylation and Preserves the Endoplasmic Reticulum Stress Response under Nitrosative Stress
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Inositol-requiring enzyme 1�� (IRE1��) is a sensor of endoplasmic reticulum (ER) stress and drives ER stress response pathways. Activated IRE1�� exhibits RNase activity and cleaves mRNA encoding X-box binding protein 1, a transcription factor that induces the expression of genes that maintain ER proteostasis for cell survival. Previously, we showed that IRE1�� undergoes S-nitrosylation, a post-translational modification induced by nitric oxide (NO), resulting in reduced RNase activity. Therefore, S-nitrosylation of IRE1�� compromises the response to ER stress, making cells more vulnerable. We conducted virtual screening and cell-based validation experiments to identify compounds that inhibit the S-nitrosylation of IRE1�� by targeting nitrosylated cysteine residues. We ultimately identified a compound (1ACTA) that selectively inhibits the S-nitrosylation of IRE1�� and prevents the NO-induced reduction of RNase activity. Furthermore, 1ACTA reduces the rate of NO-induced cell death. Our research identified S-nitrosylation as a novel target for drug development for IRE1�� and provides a suitable screening strategy.
en-copyright=
kn-copyright=

en-aut-name=KurogiHaruna
en-aut-sei=Kurogi
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KumarAshutosh
en-aut-sei=Kumar
en-aut-mei=Ashutosh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DohmaeNaoshi
en-aut-sei=Dohmae
en-aut-mei=Naoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SawadaDaisuke
en-aut-sei=Sawada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ZhangKam Y.J.
en-aut-sei=Zhang
en-aut-mei=Kam Y.J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=5
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=6
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=7
en-affil=Department of Fine Organic Synthesis, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Laboratory for Structural Bioinformatics, Center for Biosystems Dynamics Research, RIKEN
kn-affil=

affil-num=9
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=11
article-no=
start-page=4984
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250522
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Induced Pluripotent Stem Cells in Cardiomyopathy: Advancing Disease Modeling, Therapeutic Development, and Regenerative Therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Cardiomyopathies are a heterogeneous group of heart muscle diseases that can lead to heart failure, arrhythmias, and sudden cardiac death. Traditional animal models and in vitro systems have limitations in replicating the complex pathology of human cardiomyopathies. Induced pluripotent stem cells (iPSCs) offer a transformative platform by enabling the generation of patient-specific cardiomyocytes, thus opening new avenues for disease modeling, drug discovery, and regenerative therapy. This process involves reprogramming somatic cells into iPSCs and subsequently differentiating them into functional cardiomyocytes, which can be characterized using techniques such as electrophysiology, contractility assays, and gene expression profiling. iPSC-derived cardiomyocyte (iPSC-CM) platforms are also being explored for drug screening and personalized medicine, including high-throughput testing for cardiotoxicity and the identification of patient-tailored therapies. While iPSC-CMs already serve as valuable models for understanding disease mechanisms and screening drugs, ongoing advances in maturation and bioengineering are bringing iPSC-based therapies closer to clinical application. Furthermore, the integration of multi-omics approaches and artificial intelligence (AI) is enhancing the predictive power of iPSC models. iPSC-based technologies are paving the way for a new era of personalized cardiology, with the potential to revolutionize the management of cardiomyopathies through patient-specific insights and regenerative strategies.
en-copyright=
kn-copyright=

en-aut-name=VoQuan Duy
en-aut-sei=Vo
en-aut-mei=Quan Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AkagiSatoshi
en-aut-sei=Akagi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyoshiToru
en-aut-sei=Miyoshi
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=induced pluripotent stem cells
kn-keyword=induced pluripotent stem cells
en-keyword=cardiomyopathy
kn-keyword=cardiomyopathy
en-keyword=disease modeling
kn-keyword=disease modeling
en-keyword=drug screening
kn-keyword=drug screening
en-keyword=regenerative therapy
kn-keyword=regenerative therapy
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=27163
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250725
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Eosinophils as a predictive marker of treatment-related adverse events in mRCC patients treated with first-line immune-checkpoint inhibitor combination therapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Immune checkpoint inhibitors (ICIs) are a key component of first-line treatment for metastatic renal cell carcinoma (mRCC). However, predicting treatment-related adverse events (TRAEs) remains challenging. This study investigated the utility of eosinophil-related biomarkers as predictors of Common Terminology Criteria for Adverse Events grade???3 TRAEs in mRCC patients undergoing ICI combination therapy. In this retrospective analysis across 21 hospitals in Japan, we examined 180 patients treated with ICI/ICI therapy and 216 patients treated with ICI/tyrosine kinase inhibitor (TKI) therapy. Grade???3 TRAEs occurred in 39.4% and 31.9% of patients in the ICI/ICI and ICI/TKI groups, respectively. An elevated eosinophil proportion of???2.0% (odds ratio [OR]: 2.36; 95% CI [confidence interval] 1.23?4.54, p?=?0.01) and a low neutrophil/eosinophil ratio (NER) of???40.0 (OR: 2.78, 95% CI 1.39?5.53, p?=?0.004) were significant predictors of severe TRAEs in the ICI/ICI group. However, no significant associations were found in the ICI/TKI group. These findings may help identify patients who suffer from grade???3 TRAEs and help determine individualized treatment strategies in patients with mRCC.
en-copyright=
kn-copyright=

en-aut-name=KawadaTatsushi
en-aut-sei=Kawada
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatayamaSatoshi
en-aut-sei=Katayama
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YanagisawaTakafumi
en-aut-sei=Yanagisawa
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MoriKeiichiro
en-aut-sei=Mori
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FukuokayaWataru
en-aut-sei=Fukuokaya
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KomuraKazumasa
en-aut-sei=Komura
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsujinoTakuya
en-aut-sei=Tsujino
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MaenosonoRyoichi
en-aut-sei=Maenosono
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakaharaKiyoshi
en-aut-sei=Takahara
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NukayaTakuhisa
en-aut-sei=Nukaya
en-aut-mei=Takuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=InokiLan
en-aut-sei=Inoki
en-aut-mei=Lan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=ToyodaShingo
en-aut-sei=Toyoda
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=HashimotoTakeshi
en-aut-sei=Hashimoto
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=HirasawaYosuke
en-aut-sei=Hirasawa
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=EdamuraKohei
en-aut-sei=Edamura
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KobayashiTomoko
en-aut-sei=Kobayashi
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=BekkuKensuke
en-aut-sei=Bekku
en-aut-mei=Kensuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=NishimuraShingo
en-aut-sei=Nishimura
en-aut-mei=Shingo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=IwataTakehiro
en-aut-sei=Iwata
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=TominagaYusuke
en-aut-sei=Tominaga
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

en-aut-name=YamanoiTomoaki
en-aut-sei=Yamanoi
en-aut-mei=Tomoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=22
ORCID=

en-aut-name=YoshinagaKasumi
en-aut-sei=Yoshinaga
en-aut-mei=Kasumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=23
ORCID=

en-aut-name=TsuboiKazuma
en-aut-sei=Tsuboi
en-aut-mei=Kazuma
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=24
ORCID=

en-aut-name=KobayashiYasuyuki
en-aut-sei=Kobayashi
en-aut-mei=Yasuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=25
ORCID=

en-aut-name=TakamotoAtsushi
en-aut-sei=Takamoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=26
ORCID=

en-aut-name=KuroseKyohei
en-aut-sei=Kurose
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=27
ORCID=

en-aut-name=KimuraTakahiro
en-aut-sei=Kimura
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=28
ORCID=

en-aut-name=AzumaHaruhito
en-aut-sei=Azuma
en-aut-mei=Haruhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=29
ORCID=

en-aut-name=ShirokiRyoichi
en-aut-sei=Shiroki
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=30
ORCID=

en-aut-name=FujitaKazutoshi
en-aut-sei=Fujita
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=31
ORCID=

en-aut-name=OhnoYoshio
en-aut-sei=Ohno
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=32
ORCID=

en-aut-name=ArakiMotoo
en-aut-sei=Araki
en-aut-mei=Motoo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=33
ORCID=

affil-num=1
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=7
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=8
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=9
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

affil-num=10
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

affil-num=11
en-affil=Department of Urology, Kindai University Faculty of Medicine
kn-affil=

affil-num=12
en-affil=Department of Urology, Kindai University Faculty of Medicine
kn-affil=

affil-num=13
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

affil-num=14
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

affil-num=15
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=16
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=17
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=18
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=19
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=20
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=21
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=22
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=23
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=24
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=25
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=26
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=27
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=28
en-affil=Department of Urology, The Jikei University School of Medicine
kn-affil=

affil-num=29
en-affil=Department of Urology, Osaka Medical and Pharmaceutical University
kn-affil=

affil-num=30
en-affil=Department of Urology, Fujita Health University School of Medicine
kn-affil=

affil-num=31
en-affil=Department of Urology, Kindai University Faculty of Medicine
kn-affil=

affil-num=32
en-affil=Department of Urology, Tokyo Medical University
kn-affil=

affil-num=33
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Renal cell carcinoma
kn-keyword=Renal cell carcinoma
en-keyword=Immune checkpoint inhibitor
kn-keyword=Immune checkpoint inhibitor
en-keyword=ICI
kn-keyword=ICI
en-keyword=Eosinophil
kn-keyword=Eosinophil
en-keyword=Immune-related adverse event
kn-keyword=Immune-related adverse event
en-keyword=Treatment-related adverse event
kn-keyword=Treatment-related adverse event
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=10
article-no=
start-page=1444
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250516
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Canine c-kit Novel Mutation Isolated from a Gastrointestinal Stromal Tumor (GIST) Retains the Ability to Form Dimers but Lacks Autophosphorylation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors that develop in the gastrointestinal tract; KIT mutations are present in both canine and human GISTs. In this study, genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) sections of 55 canine GIST cases, and mutation searches were performed for exons 8, 9, and 11. The results revealed novel mutations, A434T and F436S, in exon 8. In contrast to the A434T mutation without functional changes, the F436S mutant retained its dimerization ability, but lost its phosphorylation function and attenuated downstream Akt signaling, which is reflected in wound healing and migration activities. A comparison of the subcellular localization of WT KIT and the F436S mutant revealed no differences. In silico simulations indicated that the F436S mutation alters the structure of the near-membrane region and that its effects may extend to the transmembrane and intracellular domains compared to the WT. F436S is a point mutation that affects the entire molecule because co-mutation with the F436S mutation and the known autophosphorylation mutation reduces the autophosphorylation abilities.
en-copyright=
kn-copyright=

en-aut-name=ShimakawaKei
en-aut-sei=Shimakawa
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DogeSo
en-aut-sei=Doge
en-aut-mei=So
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MichishitaMasaki
en-aut-sei=Michishita
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanabeEri
en-aut-sei=Tanabe
en-aut-mei=Eri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TajimaTsuyoshi
en-aut-sei=Tajima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiMasato
en-aut-sei=Kobayashi
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=BonkobaraMakoto
en-aut-sei=Bonkobara
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OchiaiKazuhiko
en-aut-sei=Ochiai
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanakaYoshikazu
en-aut-sei=Tanaka
en-aut-mei=Yoshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=2
en-affil=Laboratory of Veterinary Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=3
en-affil=Laboratory of Veterinary Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=4
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=5
en-affil=Laboratory of Veterinary Pharmacology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=6
en-affil=Laboratory of Veterinary Reproduction, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=7
en-affil=Laboratory of Veterinary Clinical Pathology, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=8
en-affil=Laboratory of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=

affil-num=10
en-affil=Laboratory of Veterinary Hygiene, School of Veterinary Science, Nippon Veterinary and Life Science University
kn-affil=
en-keyword=autophosphorylation
kn-keyword=autophosphorylation
en-keyword=canine
kn-keyword=canine
en-keyword=c-kit
kn-keyword=c-kit
en-keyword=GIST
kn-keyword=GIST
en-keyword=KIT
kn-keyword=KIT
en-keyword=loss-of-function mutation
kn-keyword=loss-of-function mutation
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=1
article-no=
start-page=2
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250128
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of temperature cycles on the sleep-like state in Hydra vulgaris
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Sleep is a conserved physiological phenomenon across species. It is mainly controlled by two processes: a circadian clock that regulates the timing of sleep and a homeostat that regulates the sleep drive. Even cnidarians, such as Hydra and jellyfish, which lack a brain, display sleep-like states. However, the manner in which environmental cues affect sleep-like states in these organisms remains unknown. In the present study, we investigated the effects of light and temperature cycles on the sleep-like state in Hydra vulgaris.<br>
Results Our findings indicate that Hydra responds to temperature cycles with a difference of up to 5�� C, resulting in decreased sleep duration under light conditions and increased sleep duration in dark conditions. Furthermore, our results reveal that Hydra prioritizes temperature changes over light as an environmental cue. Additionally, our body resection experiments show tissue-specific responsiveness in the generation ofthe sleep-like state under different environmental cues. Specifically, the upper body can generate the sleep-like state in response to a single environmental cue. In contrast, the lower body did not respond to 12-h light?dark cycles at a constant temperature.<br>
Conclusions These findings indicate that both light and temperature influence the regulation of the sleep-like state in Hydra. Moreover, these observations highlight the existence of distinct regulatory mechanisms that govern patterns of the sleep-like state in brainless organisms, suggesting the potential involvement of specific regions for responsiveness of environmental cues for regulation of the sleep-like state.
en-copyright=
kn-copyright=

en-aut-name=SatoAya
en-aut-sei=Sato
en-aut-mei=Aya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SekiguchiManabu
en-aut-sei=Sekiguchi
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakadaKoga
en-aut-sei=Nakada
en-aut-mei=Koga
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItohTaichi Q.
en-aut-sei=Itoh
en-aut-mei=Taichi Q.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Faculty of Arts and Science, Kyushu University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Systems Life Sciences, Kyushu University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Faculty of Arts and Science, Kyushu University
kn-affil=
en-keyword=Hydra
kn-keyword=Hydra
en-keyword=Sleep
kn-keyword=Sleep
en-keyword=Temperature
kn-keyword=Temperature
en-keyword=Environmental cues
kn-keyword=Environmental cues
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=10819
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A high-protein diet-responsive gut hormone regulates behavioral and metabolic optimization in Drosophila melanogaster
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Protein is essential for all living organisms; however, excessive protein intake can have adverse effects, such as hyperammonemia. Although mechanisms responding to protein deficiency are well-studied, there is a significant gap in our understanding of how organisms adaptively suppress excessive protein intake. In the present study, utilizing the fruit fly, Drosophila melanogaster, we discover that the peptide hormone CCHamide1 (CCHa1), secreted by enteroendocrine cells in response to a high-protein diet (HPD), is vital for suppressing overconsumption of protein. Gut-derived CCHa1 is received by a small subset of enteric neurons that produce short neuropeptide F, thereby modulating protein-specific satiety. Importantly, impairment of the CCHa1-mediated gut-enteric neuronal axis results in ammonia accumulation and a shortened lifespan under HPD conditions. Collectively, our findings unravel the crosstalk of gut hormone and neuronal pathways that orchestrate physiological responses to prevent and adapt to dietary protein overload.
en-copyright=
kn-copyright=

en-aut-name=YoshinariYuto
en-aut-sei=Yoshinari
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishimuraTakashi
en-aut-sei=Nishimura
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoShu
en-aut-sei=Kondo
en-aut-mei=Shu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TanimotoHiromu
en-aut-sei=Tanimoto
en-aut-mei=Hiromu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KobayashiTomoe
en-aut-sei=Kobayashi
en-aut-mei=Tomoe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NiwaRyusuke
en-aut-sei=Niwa
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=2
en-affil=Metabolic Regulation and Genetics, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biological Science and Technology, Faculty of Advanced Engineering, Tokyo University of Science
kn-affil=

affil-num=5
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=6
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=7
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=8
en-affil=Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (TARA), University of Tsukuba
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250710
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurotransmitter and Receptor Mapping in Drosophila Circadian Clock Neurons via T2A-GAL4 Screening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The circadian neuronal network in the brain comprises central pacemaker neurons and associated input and output pathways. These components work together to generate coherent rhythmicity, synchronize with environmental time cues, and convey circadian information to downstream neurons that regulate behaviors such as the sleep/wake cycle. To mediate these functions, neurotransmitters and neuromodulators play essential roles in transmitting and modulating signals between neurons. In Drosophila melanogaster, approximately 240 brain neurons function as clock neurons. Previous studies have identified several neurotransmitters and neuromodulators, including the Pigment-dispersing factor (PDF) neuropeptide, along with their corresponding receptors in clock neurons. However, our understanding of the neurotransmitters and receptors involved in the circadian system remains incomplete. In this study, we conducted a T2A-GAL4-based screening for neurotransmitter and receptor genes expressed in clock neurons. We identified 2 neurotransmitter-related genes and 22 receptor genes. Notably, while previous studies had reported the expression of 6 neuropeptide receptor genes in large ventrolateral neurons (l-LNv), we also found that 14 receptor genes?including those for dopamine, serotonin, and ��-aminobutyric acid?are expressed in l-LNv neurons. These findings suggest that l-LNv neurons serve as key integrative hubs within the circadian network, receiving diverse external signals.
en-copyright=
kn-copyright=

en-aut-name=FukudaAyumi
en-aut-sei=Fukuda
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoAika
en-aut-sei=Saito
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=clock neurons
kn-keyword=clock neurons
en-keyword=neurotransmitter
kn-keyword=neurotransmitter
en-keyword=T2A-GAL4
kn-keyword=T2A-GAL4
en-keyword=immunostaining
kn-keyword=immunostaining
en-keyword=Drosophila
kn-keyword=Drosophila
END

start-ver=1.4
cd-journal=joma
no-vol=35
cd-vols=
no-issue=12
article-no=
start-page=2916
end-page=2926.e3
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202506
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Oxytocin facilitates human touch-induced play behavior in rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Pleasant touch sensations play a fundamental role in social bonding, yet the neural mechanisms underlying affinity-like behaviors remain poorly understood. Here, we demonstrate that juvenile-adolescent rats, which naturally engage in social play with peers characterized by rough-and-tumble interactions and 50 kHz ultrasonic vocalizations indicating pleasant sensations, develop a strong affinity for human hands through similar playful contact achieved by repeated tickling with human hands. Using this rat with tickling-induced high affinity for human hands, we discovered that repeated tickling mimicking rough-and-tumble play led to increased oxytocin receptor (OTR) expression in the ventrolateral part of the ventromedial hypothalamus (VMHvl). Inhibition of oxytocin signaling in the VMHvl reduced affinity-like behaviors from rats to human hands. These findings suggest that OTR neurons in VMHvl play an important role in the increase in affinity for human hands induced by pleasant touch sensation with human touch-induced play behavior. Based on retrograde and anterograde tracing studies examining the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) as primary sources of oxytocin, we demonstrate that a subset of oxytocin fibers in the VMHvl originate from the SON, suggesting that affinity-like behavior from rats to human hands may be controlled by oxytocin signaling from magnocellular neurons. Together, this work advances our understanding of how oxytocin shapes social behavior and may inform the development of therapeutic strategies to promote positive social interactions.
en-copyright=
kn-copyright=

en-aut-name=HayashiHimeka
en-aut-sei=Hayashi
en-aut-mei=Himeka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TateishiSayaka
en-aut-sei=Tateishi
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InutsukaAyumu
en-aut-sei=Inutsuka
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaejimaSho
en-aut-sei=Maejima
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HagiwaraDaisuke
en-aut-sei=Hagiwara
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakumaYasuo
en-aut-sei=Sakuma
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=OnakaTatsushi
en-aut-sei=Onaka
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GrinevichValery
en-aut-sei=Grinevich
en-aut-mei=Valery
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=4
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=6
en-affil=Department of Anatomy and Neurobiology, Graduate School of Medical Sciences, Nippon Medical School
kn-affil=

affil-num=7
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=

affil-num=8
en-affil=Department of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, German Center for Psychiatry (DZPG), Medical Faculty Mannheim, University of Heidelberg
kn-affil=

affil-num=9
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University,
kn-affil=
en-keyword=tickling
kn-keyword=tickling
en-keyword=oxytocin
kn-keyword=oxytocin
en-keyword=oxytocin receptor
kn-keyword=oxytocin receptor
en-keyword=ventrolateral part of the ventromedial hypothalamus
kn-keyword=ventrolateral part of the ventromedial hypothalamus
en-keyword=affinity-like behaviors
kn-keyword=affinity-like behaviors
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=7
article-no=
start-page=808
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NAD+ Cleavage Activity, Ameliorates Symptoms of Peripheral Neuropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a nicotinamide adenine dinucleotide (NAD+) hydrolase involved in axonal degeneration and neuronal cell death. SARM1 plays a pivotal role in triggering the neurodegenerative processes that underlie peripheral neuropathies, traumatic brain injury, and neurodegenerative diseases. Importantly, SARM1 knockdown or knockout prevents the degeneration; as a result, SARM1 has been attracting attention as a potent therapeutic target. In recent years, the development of several SARM1 inhibitors derived from synthetic chemical compounds has been reported; however, no dietary ingredients with SARM1 inhibitory activity have been identified. Therefore, we here focused on dietary ingredients and found that carnosol, an antioxidant contained in rosemary, inhibits the NAD+-cleavage activity of SARM1. Purified carnosol inhibited the enzymatic activity of SARM1 and suppressed neurite degeneration and cell death induced by the anti-cancer medicine vincristine (VCR). Carnosol also inhibited VCR-induced hyperalgesia symptoms, suppressed the loss of intra-epidermal nerve fibers in vivo, and reduced the blood fluid level of phosphorylated neurofilament-H caused by an axonal degeneration event. These results indicate that carnosol has a neuroprotective effect via SARM1 inhibition in addition to its previously known antioxidant effect via NF-E2-related factor 2 and thus suppresses neurotoxin-induced peripheral neuropathy.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OgawaKazuki
en-aut-sei=Ogawa
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuiYu
en-aut-sei=Yasui
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamamotoKen-Ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-Ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaYoji
en-aut-sei=Wada
en-aut-mei=Yoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakamuraHiromichi
en-aut-sei=Nakamura
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=9
en-affil=Tama Biochemical Co., Ltd.
kn-affil=

affil-num=10
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=SARM1
kn-keyword=SARM1
en-keyword=carnosol
kn-keyword=carnosol
en-keyword=NAD+
kn-keyword=NAD+
en-keyword=axon degeneration
kn-keyword=axon degeneration
en-keyword=peripheral neuropathy
kn-keyword=peripheral neuropathy
END

start-ver=1.4
cd-journal=joma
no-vol=7
cd-vols=
no-issue=1
article-no=
start-page=e000923
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250427
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Reversible cerebral vasoconstriction syndrome in idiopathic multicentric Castleman disease under treatment with tocilizumab
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Idiopathic multicentric Castleman disease (iMCD) is a rare polyclonal lymphoproliferative disorder characterised by systemic inflammation resulting from overproduction of interleukin 6 (IL-6). While iMCD primarily affects the lymph nodes and related tissues, it can also rarely involve the central nervous system.<br>
Case presentation We report the case of a 58-year-old female patient with at least a 3-year history of iMCD, who experienced acute thunderclap headaches due to reversible cerebral vasoconstriction syndrome (RCVS). RCVS occurred 3?months after initiating treatment with tocilizumab, a humanised anti-IL-6 receptor monoclonal antibody, and was accompanied by focal cortical subarachnoid haemorrhage (SAH). Elevated IL-6 levels were found in both serum and cerebrospinal fluid. MR angiography revealed multiple diffuse stenotic lesions in the bilateral middle and posterior cerebral arteries, which, along with bilateral cerebral oedema, resolved within 3?months. The diffuse nature of the cerebral vasospasm and the presence of bilateral brain oedema suggested that cerebral vasospasm was due to RCVS rather than SAH.<br>
Conclusions In patients with Castleman disease, RCVS may occur due to IL-6-dependent chronic cerebral vascular inflammation, either as a primary condition or as a complication of tocilizumab treatment.
en-copyright=
kn-copyright=

en-aut-name=KamimuraNaoya
en-aut-sei=Kamimura
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UedaNaohisa
en-aut-sei=Ueda
en-aut-mei=Naohisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraKatsuo
en-aut-sei=Kimura
en-aut-mei=Katsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NishikoriAsami
en-aut-sei=Nishikori
en-aut-mei=Asami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SatoYasuharu
en-aut-sei=Sato
en-aut-mei=Yasuharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KishidaHitaru
en-aut-sei=Kishida
en-aut-mei=Hitaru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TanakaFumiaki
en-aut-sei=Tanaka
en-aut-mei=Fumiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=2
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=3
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=4
en-affil=
kn-affil=

affil-num=5
en-affil=
kn-affil=

affil-num=6
en-affil=Department of Neurology, Yokohama City University Medical Center
kn-affil=

affil-num=7
en-affil=Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250624
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Dual functions of SNAP25 in mouse taste buds
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Type III cells in mouse taste buds are considered to transmit aversive stimuli, such as sourness, to the gustatory nerve through vesicular synapses. Synaptosome-associated protein 25 (SNAP25) might contribute to synaptic vesicular release in sour sensation, although direct evidence has been lacking. Here, we demonstrated that epithelia-specific Snap25 conditional knockout (cKO) mice exhibited a significant reduction in the number of type III cells. Notably, the proportion of 5-ethynyl 2��-deoxyuridine-positive post-mitotic type III cells in Snap25 cKO mice was significantly lower on tracing day 14, but not at day 7, which suggests that SNAP25 contributes to the maintenance of type III cells. In a short-term lick test, Snap25 cKO (sour taste absent) and Snap25/ transient receptor potential vanilloid 1 double KO (sour taste and somatosensory absent) mice exhibit a significantly higher lick response to sour tastants, confirming the role of SNAP25 for sour sensation. Electrophysiological recordings of the chorda tympani nerve reveal nearly abolished ammonium and sour taste responses in Snap25 cKO mice, which concludes sour-dependent synapse transmission in type III cells. Overall, these data suggest that vesicular synapses in taste buds are indispensable for transmission of information from, and the replenishment of, sour-sensitive type III taste cells.
en-copyright=
kn-copyright=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangKuanyu
en-aut-sei=Wang
en-aut-mei=Kuanyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HuangHai
en-aut-sei=Huang
en-aut-mei=Hai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YasumatsuKeiko
en-aut-sei=Yasumatsu
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Tokyo Dental Junior College
kn-affil=

affil-num=5
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=sour taste
kn-keyword=sour taste
en-keyword=synapse
kn-keyword=synapse
en-keyword=taste buds
kn-keyword=taste buds
en-keyword=taste nerve
kn-keyword=taste nerve
en-keyword=Type III cells
kn-keyword=Type III cells
END

start-ver=1.4
cd-journal=joma
no-vol=166
cd-vols=
no-issue=8
article-no=
start-page=bqaf102
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neuromedin U Deficiency Disrupts Daily Testosterone Fluctuation and Reduces Wheel-running Activity in Rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The objective of this study was to elucidate the role of endogenous Neuromedin U (NMU) in rats by performing NMU knockout (KO). Male, but not female NMU KO rats exhibited decreased wheel-running activity vs wildtype (WT), although overall home cage activity was not affected. Plasma testosterone in WT rats varied significantly over the course of a day, with a peak at ZT1 and a nadir at ZT18, whereas in NMU KO rats testosterone remained stable throughout the day. Chronic administration of testosterone restored wheel-running activity in NMU KO rats to the same level as in WT rats, suggesting that the decrease in wheel-running activity in NMU KO rats is due to the disruption of the diurnal change of testosterone. Accordingly, expression of the luteinizing hormone beta subunit (Lhb) mRNA in the pars distalis of anterior pituitary was significantly lower in NMU KO rats; immunostaining revealed that the size of luteinizing hormone (LH)?expressing cells was also relatively small in those animals. In the brain of male WT rats, Nmu was highly expressed in the pars tuberalis, and the NMU receptor Nmur2 was highly expressed in the ependymal cell layer of the third ventricle. This study reveals a novel function of NMU and indicates that endogenous NMU in rats plays a role in the regulation of motivated activity via regulation of testosterone.
en-copyright=
kn-copyright=

en-aut-name=OtsukaMai
en-aut-sei=Otsuka
en-aut-mei=Mai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakeuchiYu
en-aut-sei=Takeuchi
en-aut-mei=Yu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MoriyamaMaho
en-aut-sei=Moriyama
en-aut-mei=Maho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EgoshiSakura
en-aut-sei=Egoshi
en-aut-mei=Sakura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=GotoYuki
en-aut-sei=Goto
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GuTingting
en-aut-sei=Gu
en-aut-mei=Tingting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KimuraAtsushi P
en-aut-sei=Kimura
en-aut-mei=Atsushi P
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HaraguchiShogo
en-aut-sei=Haraguchi
en-aut-mei=Shogo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakeuchiSakae
en-aut-sei=Takeuchi
en-aut-mei=Sakae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MatsuyamaMakoto
en-aut-sei=Matsuyama
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BentleyGeorge E
en-aut-sei=Bentley
en-aut-mei=George E
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=AizawaSayaka
en-aut-sei=Aizawa
en-aut-mei=Sayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Biology, Faculty of Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Biological Sciences, Faculty of Science, Hokkaido University
kn-affil=

affil-num=8
en-affil=Department of Biochemistry, Showa University School of Medicine
kn-affil=

affil-num=9
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=11
en-affil=Division of Molecular Genetics, Shigei Medical Research Institute
kn-affil=

affil-num=12
en-affil=Department of Integrative Biology and Helen Wills Neuroscience Institute, University of California at Berkeley
kn-affil=

affil-num=13
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Neuromedin U
kn-keyword=Neuromedin U
en-keyword=rat
kn-keyword=rat
en-keyword=motivation
kn-keyword=motivation
en-keyword=activity
kn-keyword=activity
en-keyword=testosterone
kn-keyword=testosterone
en-keyword=wheel-running
kn-keyword=wheel-running
END

start-ver=1.4
cd-journal=joma
no-vol=64
cd-vols=
no-issue=5
article-no=
start-page=759
end-page=762
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Novel De Novo Variant in KCNH5 in a Patient with Refractory Epileptic Encephalopathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We herein report a novel de novo KCNH5 variant in a patient with refractory epileptic encephalopathy. The patient exhibited seizures at 1 year and 7 months old, which gradually worsened, leading to a bedridden status. Brain magnetic resonance imaging (MRI) showed cerebral atrophy and cerebellar hypoplasia. A trio whole-exome sequence analysis identified a de novo heterozygous c.640A>C, p.Lys214Gln variant in KCNH5 that was predicted to be deleterious. Recent studies have linked KCNH5 to various epileptic encephalopathies, with many patients showing normal MRI findings. The present case expands the clinical spectrum of the disease, as it is characterized by severe neurological prognosis, cerebral atrophy, and cerebellar hypoplasia.
en-copyright=
kn-copyright=

en-aut-name=MitsutakeAkihiko
en-aut-sei=Mitsutake
en-aut-mei=Akihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukawaTakashi
en-aut-sei=Matsukawa
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaitoTatsuhiko
en-aut-sei=Naito
en-aut-mei=Tatsuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MitsuiJun
en-aut-sei=Mitsui
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HaradaHiroaki
en-aut-sei=Harada
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujioKeishi
en-aut-sei=Fujio
en-aut-mei=Keishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=FujishiroJun
en-aut-sei=Fujishiro
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MoriHarushi
en-aut-sei=Mori
en-aut-mei=Harushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MorishitaShinichi
en-aut-sei=Morishita
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=6
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=7
en-affil=Department of Rheumatology and Allergy, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Department of Pediatric Surgery, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=9
en-affil=Department of Radiology, School of Medicine, Jichi Medical University
kn-affil=

affil-num=10
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
en-keyword=epileptic encephalopathy
kn-keyword=epileptic encephalopathy
en-keyword=whole-exome sequencing
kn-keyword=whole-exome sequencing
en-keyword=KCNH5
kn-keyword=KCNH5
en-keyword=de novo variant
kn-keyword=de novo variant
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recent progress in oculopharyngodistal myopathy research from clinical and genetic viewpoints
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Oculopharyngodistal myopathy (OPDM) is a rare muscular disorder characterized by ocular symptoms, pharyngeal symptoms, facial weakness, and distal predominant limb muscle weakness. The cause of the disease was unknown for a long time. Recently, however, it has been reported that expansions of CGG or CCG repeats in LRP12, LOC642361/NUTM2B-AS1, GIPC1, NOTCH2NLC, RILPL1, and ABCD3 are the causes of the disease. Cases sometimes present with neurological symptoms, and the clinical spectrum of diseases caused by expansions of CGG or CCG repeats has been proposed to be called FNOP-spectrum disorder after the names of fragile X-associated tremor/ataxia syndrome, neuronal intranuclear inclusion disease, oculopharyngeal myopathy with leukoencephalopathy, and OPDM. In this article, the recent progress in the field of OPDM is reviewed, and remaining issues in OPDM are discussed.
en-copyright=
kn-copyright=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=oculopharyngodistal myopathy
kn-keyword=oculopharyngodistal myopathy
en-keyword=CGG repeat
kn-keyword=CGG repeat
en-keyword=CCG repeat
kn-keyword=CCG repeat
en-keyword=repeat motif?phenotype correlation
kn-keyword=repeat motif?phenotype correlation
en-keyword=FNOP-spectrum disorder
kn-keyword=FNOP-spectrum disorder
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=5602-25
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=2025
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Two Cases of Autosomal Recessive Spinocerebellar Ataxia-8 Showing Two Novel Variants of SYNE1 in Japanese Families
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Autosomal recessive spinocerebellar ataxia-8 (SCAR8) is a neurodegenerative disorder caused by the biallelic pathogenic variants of SYNE1. It is characterized by slowly progressive cerebellar ataxia and atrophy. We identified two SCAR8 families using exome analyses and two novel variants, c.2127delG (p.Met709Ilefs) and c.15943G>T (p.Gly5315*), in SYNE1 (NM_182961.4). Pathogenic variants of SYNE1 cause various symptoms, including cerebellar ataxia, pyramidal tract disorders, and joint disorders, and the pathogenic variants discovered in this study were located in a region prone to cerebellar ataxia.
en-copyright=
kn-copyright=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsakadaYosuke
en-aut-sei=Osakada
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
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en-aut-name=OTA ELLIOTT RICARDO SATOSHI
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affil-num=1
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en-aut-name=XUSHANSHAN
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affil-num=1
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en-title=�z���Ґ��h���Ö@��CCL2������o�H��}�����邱�ƂłĂ񂩂񃂃f�����b�g�ɑ΂��čR�Ă񂩂��p������
kn-title=Cervical spinal cord stimulation exerts anti-epileptic effects in a rat model of epileptic seizure through the suppression of CCL2-mediated cascades
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en-aut-name=OKAZAKIYosuke
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aut-affil-num=1
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affil-num=1
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cd-journal=joma
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start-page=715
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kn-title=TRPV2 mediates stress resilience in mouse cardiomyocytes
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kn-abstract=The heart dynamically compensates for haemodynamic stress, but how this resilience forms during cardiac growth is not clear. Using a temporally inducible, cardiac-specific knockout in mice we show that the Transient receptor potential vanilloid family 2 (TRPV2) channel is crucial for the maturation of cardiomyocyte stress resilience. TRPV2 defects in growing hearts lead to small morphology, abnormal intercalated discs, weak contractility, and low expression of serum response factor and Insulin-like growth factor-1 (IGF-1) signalling. Individual cardiomyocytes of TRPV2-deficient hearts show reduced contractility with abnormal Ca2+ handling. In cultured neonatal cardiomyocytes, mechanical Ca2+ response, excitation-contraction coupling, sarcoplasmic reticulum Ca2+ content, actin formation, nuclear localisation of Myocyte enhancer factor 2c, and IGF-1 expression require TRPV2. TRPV2-deficient hearts show a defective response to dobutamine stress and no compensatory hypertrophic response to phenylephrine administration, but no stress response to pressure overload. These data suggest TRPV2 mediates the maturation of cardiomyocyte stress resilience, and will advance therapeutic interventions and drug discovery for heart disease.
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en-aut-name=DongYubing
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en-aut-name=WangGuohao
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en-aut-name=UjiharaYoshihiro
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en-aut-name=ChenYanzhu
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aut-affil-num=4
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en-aut-name=YoshidaMasashi
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en-aut-name=NakamuraKazufumi
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en-aut-name=KatanosakaKimiaki
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en-aut-name=NaruseKeiji
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en-aut-name=KatanosakaYuki
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aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Electrical and Mechanical Engineering, Graduate School of Engineering, Nagoya Institute of Technology
kn-affil=

affil-num=4
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Biomedical Sciences, College of Life and Health Sciences, Chubu University
kn-affil=

affil-num=8
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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END

start-ver=1.4
cd-journal=joma
no-vol=214
cd-vols=
no-issue=
article-no=
start-page=32
end-page=41
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202505
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Medaka approach to evolutionary social neuroscience
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Previously, the integration of comparative biological and neuroscientific approaches has led to significant advancements in social neuroscience. This review highlights the potential and future directions of evolutionary social neuroscience research utilizing medaka fishes (the family Adrianichthyidae) including Japanese medaka (Oryzias latipes). We focus on medaka social cognitive capabilities and mate choice behavior, particularly emphasizing mate preference using visual cues. Medaka fishes are also advantageous due to their abundant genetic resources, extensive genomic information, and the relative ease of laboratory breeding and genetic manipulation. Here we present some research examples of both the conventional neuroscience approach and evolutionary approach involving medaka fishes and other species. We also discuss the prospects of uncovering the molecular and cellular mechanisms underlying the diversity of visual mate preference among species. Especially, we introduce that the single-cell transcriptome technology, particularly in conjunction with 'Adaptive Circuitry Census', is an innovative tool that bridges comparative biological methods and neuroscientific approaches. Evolutionary social neuroscience research using medaka has the potential to unveil fundamental principles in neuroscience and elucidate the mechanisms responsible for generating diversity in mating strategies.
en-copyright=
kn-copyright=

en-aut-name=AnsaiSatoshi
en-aut-sei=Ansai
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=Hiraki-KajiyamaTowako
en-aut-sei=Hiraki-Kajiyama
en-aut-mei=Towako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UedaRyutaro
en-aut-sei=Ueda
en-aut-mei=Ryutaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SekiTakahide
en-aut-sei=Seki
en-aut-mei=Takahide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YokoiSaori
en-aut-sei=Yokoi
en-aut-mei=Saori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KatsumuraTakafumi
en-aut-sei=Katsumura
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakeuchiHideaki
en-aut-sei=Takeuchi
en-aut-mei=Hideaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Ushimado Marine Institute, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=3
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=4
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=

affil-num=5
en-affil=School of Pharmaceutical Sciences, Hokkaido University
kn-affil=

affil-num=6
en-affil=School of Medicine, Kitasato University
kn-affil=

affil-num=7
en-affil=Graduate School of Life Sciences, Tohoku University
kn-affil=
en-keyword=Evolutionary neuroscience
kn-keyword=Evolutionary neuroscience
en-keyword=Comparative neuroscience
kn-keyword=Comparative neuroscience
en-keyword=Medaka bioresource
kn-keyword=Medaka bioresource
en-keyword=Visual mate preference
kn-keyword=Visual mate preference
en-keyword=Sexual selection
kn-keyword=Sexual selection
en-keyword=Genetic manipulation
kn-keyword=Genetic manipulation
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=7
article-no=
start-page=2221
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Length Estimation of Pneumatic Artificial Muscle with Optical Fiber Sensor Using Machine Learning
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A McKibben artificial muscle is a soft actuator driven by air pressure, characterized by its flexibility, lightweight design, and high power-to-weight ratio. We have developed a smart artificial muscle that is capable of sensing its motion. To enable this sensing function, an optical fiber was integrated into the sleeve consisting of multiple fibers and serving as a component of the McKibben artificial muscle. By measuring the macrobending loss of the optical fiber, the length of the smart artificial muscle is expected to be estimated. However, experimental results indicated that the sensor's characteristics depend not only on the length but also on the load and the applied air pressure. This dependency arises because the stress applied to the optical fiber increases, causing microbending loss. In this study, we employed a machine learning model, primarily composed of Long Short-Term Memory (LSTM) neural networks, to estimate the length of the smart artificial muscle. The experimental results demonstrate that the length estimation obtained through machine learning exhibits a smaller error. This suggests that machine learning is a feasible approach to enhancing the length measurement accuracy of the smart artificial muscle.
en-copyright=
kn-copyright=

en-aut-name=NiYilei
en-aut-sei=Ni
en-aut-mei=Yilei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WakimotoShuichi
en-aut-sei=Wakimoto
en-aut-mei=Shuichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TianWeihang
en-aut-sei=Tian
en-aut-mei=Weihang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TodaYuichiro
en-aut-sei=Toda
en-aut-mei=Yuichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KandaTakefumi
en-aut-sei=Kanda
en-aut-mei=Takefumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YamaguchiDaisuke
en-aut-sei=Yamaguchi
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=McKibben artificial muscle
kn-keyword=McKibben artificial muscle
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=optical fiber
kn-keyword=optical fiber
en-keyword=motion estimation
kn-keyword=motion estimation
END

start-ver=1.4
cd-journal=joma
no-vol=213
cd-vols=
no-issue=
article-no=
start-page=128
end-page=137
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202504
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The potential mechanism maintaining transactive response DNA binding protein 43?kDa in the mouse stroke model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The disruption of transactive response DNA binding protein 43?kDa (TDP-43) shuttling leads to the depletion of nuclear localization and the cytoplasmic accumulation of TDP-43. We aimed to evaluate the mechanism underlying the behavior of TDP-43 in ischemic stroke. Adult male C57BL/6?J mice were subjected to 30 or 60?min of transient middle cerebral artery occlusion (tMCAO), and examined at 1, 6, and 24?h post reperfusion. Immunostaining was used to evaluate the expression of TDP-43, G3BP1, HDAC6, and RAD23B. The total and cytoplasmic number of TDP-43?positive cells increased compared with sham operation group and peaked at 6?h post reperfusion after tMCAO. The elevated expression of G3BP1 protein peaked at 6?h after reperfusion and decreased at 24?h after reperfusion in ischemic mice brains. We also observed an increase of expression level of HDAC6 and the number of RAD23B-positive cells increased after tMCAO. RAD23B was colocalized with TDP-43 24?h after tMCAO. We proposed that the formation of stress granules might be involved in the mislocalization of TDP-43, based on an evaluation of G3BP1 and HDAC6. Subsequently, RAD23B, may also contribute to the downstream degradation of mislocalized TDP-43 in mice tMCAO model.
en-copyright=
kn-copyright=

en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Ota-ElliottRicardo Satoshi
en-aut-sei=Ota-Elliott
en-aut-mei=Ricardo Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BianZhihong
en-aut-sei=Bian
en-aut-mei=Zhihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhaiYun
en-aut-sei=Zhai
en-aut-mei=Yun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YuHaibo
en-aut-sei=Yu
en-aut-mei=Haibo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HuXiao
en-aut-sei=Hu
en-aut-mei=Xiao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=AnHangping
en-aut-sei=An
en-aut-mei=Hangping
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=LiuHongzhi
en-aut-sei=Liu
en-aut-mei=Hongzhi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=TDP-43
kn-keyword=TDP-43
en-keyword=ALS
kn-keyword=ALS
en-keyword=RNA-binding protein
kn-keyword=RNA-binding protein
en-keyword=Mislocalization
kn-keyword=Mislocalization
en-keyword=G3BP1
kn-keyword=G3BP1
en-keyword=HDAC6
kn-keyword=HDAC6
en-keyword=RAD23B
kn-keyword=RAD23B
en-keyword=tMCAO
kn-keyword=tMCAO
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=6
article-no=
start-page=2485
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Vesicular Glutamate Transporter 3 Is Involved in Glutamatergic Signalling in Podocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glomerular podocytes act as a part of the filtration barrier in the kidney. The activity of this filter is regulated by ionotropic and metabotropic glutamate receptors. Adjacent podocytes can potentially release glutamate into the intercellular space; however, little is known about how podocytes release glutamate. Here, we demonstrated vesicular glutamate transporter 3 (VGLUT3)-dependent glutamate release from podocytes. Immunofluorescence analysis revealed that rat glomerular podocytes and an immortal mouse podocyte cell line (MPC) express VGLUT1 and VGLUT3. Consistent with this finding, quantitative RT-PCR revealed the expression of VGLUT1 and VGLUT3 mRNA in undifferentiated and differentiated MPCs. In addition, the exocytotic proteins vesicle-associated membrane protein 2, synapsin 1, and synaptophysin 1 were present in punctate patterns and colocalized with VGLUT3 in MPCs. Interestingly, approximately 30% of VGLUT3 colocalized with VGLUT1. By immunoelectron microscopy, VGLUT3 was often observed around clear vesicle-like structures in differentiated MPCs. Differentiated MPCs released glutamate following depolarization with high potassium levels and after stimulation with the muscarinic agonist pilocarpine. The depletion of VGLUT3 in MPCs by RNA interference reduced depolarization-dependent glutamate release. These results strongly suggest that VGLUT3 is involved in glutamatergic signalling in podocytes and may be a new drug target for various kidney diseases.
en-copyright=
kn-copyright=

en-aut-name=NishiiNaoko
en-aut-sei=Nishii
en-aut-mei=Naoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KawaiTomoko
en-aut-sei=Kawai
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuokaHiroki
en-aut-sei=Yasuoka
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeTadashi
en-aut-sei=Abe
en-aut-mei=Tadashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TatsumiNanami
en-aut-sei=Tatsumi
en-aut-mei=Nanami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HaradaYuika
en-aut-sei=Harada
en-aut-mei=Yuika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=LiShunai
en-aut-sei=Li
en-aut-mei=Shunai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsukanoMoemi
en-aut-sei=Tsukano
en-aut-mei=Moemi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OgawaDaisuke
en-aut-sei=Ogawa
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TakeiKohji
en-aut-sei=Takei
en-aut-mei=Kohji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=YamadaHiroshi
en-aut-sei=Yamada
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Genomics and Proteomics, Advanced Science Research Center, Okayama University
kn-affil=

affil-num=8
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Central Research Laboratory, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Neuroscience, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=VGLUT3
kn-keyword=VGLUT3
en-keyword=glutamate
kn-keyword=glutamate
en-keyword=podocyte
kn-keyword=podocyte
en-keyword=glutamatergic transmission
kn-keyword=glutamatergic transmission
END

start-ver=1.4
cd-journal=joma
no-vol=26
cd-vols=
no-issue=6
article-no=
start-page=2713
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250318
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Involvement of a Novel Variant of FGFR1 Detected in an Adult Patient with Kallmann Syndrome in Regulation of Gonadal Steroidogenesis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Fibroblast growth factor receptor 1 (FGFR1), also known as KAL2, is a tyrosine kinase receptor, and variants of FGFR1 have been detected in patients with Kallmann syndrome (KS), which is a congenital developmental disorder characterized by central hypogonadism and anosmia. Herein, we report an adult case of KS with a novel variant of FGFR1. A middle-aged male was referred for a compression fracture of a lumbar vertebra. It was shown that he had severe osteoporosis, anosmia, gynecomastia, and a past history of operations for cryptorchidism. Endocrine workup using pituitary and gonadal stimulation tests revealed the presence of both primary and central hypogonadism. Genetic testing revealed a novel variant of FGFR1 (c.2197_2199dup, p.Met733dup). To identify the pathogenicity of the novel variant and the clinical significance for the gonads, we investigated the effects of the FGFR1 variant on the downstream signaling of FGFR1 and gonadal steroidogenesis by using human steroidogenic granulosa cells. It was revealed that the transfection of the variant gene significantly impaired FGFR1 signaling, detected through the downregulation of SPRY2, compared with that of the case of the forced expression of wild-type FGFR1, and that the existence of the variant gene apparently altered the expression of key steroidogenic factors, including StAR and aromatase, in the gonad. The results suggested that the novel variant of FGFR1 detected in the patient with KS was linked to the impairment of FGFR1 signaling, as well as the alteration of gonadal steroidogenesis, leading to the pathogenesis of latent primary hypogonadism.
en-copyright=
kn-copyright=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KawaguchiMarina
en-aut-sei=Kawaguchi
en-aut-mei=Marina
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OguniKohei
en-aut-sei=Oguni
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YasudaMiho
en-aut-sei=Yasuda
en-aut-mei=Miho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HasegawaKosei
en-aut-sei=Hasegawa
en-aut-mei=Kosei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=IwataNahoko
en-aut-sei=Iwata
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=fibroblast growth factor receptor 1 (FGFR1)
kn-keyword=fibroblast growth factor receptor 1 (FGFR1)
en-keyword=gynecomastia
kn-keyword=gynecomastia
en-keyword=Kallmann syndrome (KS)
kn-keyword=Kallmann syndrome (KS)
en-keyword=osteoporosis and steroidogenesis
kn-keyword=osteoporosis and steroidogenesis
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=
article-no=
start-page=1537615
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250311
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PARylation-mediated post-transcriptional modifications in cancer immunity and immunotherapy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Poly-ADP-ribosylation (PARylation) is a post-translational modification in which ADP-ribose is added to substrate proteins. PARylation is mediated by a superfamily of ADP-ribosyl transferases known as PARPs and influences a wide range of cellular functions, including genome integrity maintenance, and the regulation of proliferation and differentiation. We and others have recently reported that PARylation of SH3 domain-binding protein 2 (3BP2) plays a role in bone metabolism, immune system regulation, and cytokine production. Additionally, PARylation has recently gained attention as a target for cancer treatment. In this review, we provide an overview of PARylation, its involvement in several signaling pathways related to cancer immunity, and the potential of combination therapies with PARP inhibitors and immune checkpoint inhibitors.
en-copyright=
kn-copyright=

en-aut-name=MatsumotoKazuya
en-aut-sei=Matsumoto
en-aut-mei=Kazuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsumotoYoshinori
en-aut-sei=Matsumoto
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=PARylation
kn-keyword=PARylation
en-keyword=cancer
kn-keyword=cancer
en-keyword=post-transcriptional regulation
kn-keyword=post-transcriptional regulation
en-keyword=ubiquitylation
kn-keyword=ubiquitylation
en-keyword=immune system
kn-keyword=immune system
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=6
article-no=
start-page=790
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Improving Diagnostic Performance for Head and Neck Tumors with Simple Diffusion Kurtosis Imaging and Machine Learning Bi-Parameter Analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Objectives: Mean kurtosis (MK) values in simple diffusion kurtosis imaging (SDI)-a type of diffusion kurtosis imaging (DKI)-have been reported to be useful in the diagnosis of head and neck malignancies, for which pre-processing with smoothing filters has been reported to improve the diagnostic accuracy. Multi-parameter analysis using DKI in combination with other image types has recently been reported to improve the diagnostic performance. The purpose of this study was to evaluate the usefulness of machine learning (ML)-based multi-parameter analysis using the MK and apparent diffusion coefficient (ADC) values-which can be acquired simultaneously through SDI-for the differential diagnosis of benign and malignant head and neck tumors, which is important for determining the treatment strategy, as well as examining the usefulness of filter pre-processing. Methods: A total of 32 pathologically diagnosed head and neck tumors were included in the study, and a Gaussian filter was used for image pre-processing. MK and ADC values were extracted from pixels within the tumor area and used as explanatory variables. Five ML algorithms were used to create models for the prediction of tumor status (benign or malignant), which were evaluated through ROC analysis. Results: Bi-parameter analysis with gradient boosting achieved the best diagnostic performance, with an AUC of 0.81. Conclusions: The usefulness of bi-parameter analysis with ML methods for the differential diagnosis of benign and malignant head and neck tumors using SDI data were demonstrated.
en-copyright=
kn-copyright=

en-aut-name=YoshidaSuzuka
en-aut-sei=Yoshida
en-aut-mei=Suzuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KurodaMasahiro
en-aut-sei=Kuroda
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakamuraYoshihide
en-aut-sei=Nakamura
en-aut-mei=Yoshihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FukumuraYuka
en-aut-sei=Fukumura
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakamitsuYuki
en-aut-sei=Nakamitsu
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Al-HammadWlla E.
en-aut-sei=Al-Hammad
en-aut-mei=Wlla E.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KurodaKazuhiro
en-aut-sei=Kuroda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShimizuYudai
en-aut-sei=Shimizu
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TanabeYoshinori
en-aut-sei=Tanabe
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OitaMasataka
en-aut-sei=Oita
en-aut-mei=Masataka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SugiantoIrfan
en-aut-sei=Sugianto
en-aut-mei=Irfan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=BarhamMajd
en-aut-sei=Barham
en-aut-mei=Majd
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TekikiNouha
en-aut-sei=Tekiki
en-aut-mei=Nouha
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KamaruddinNurul N.
en-aut-sei=Kamaruddin
en-aut-mei=Nurul N.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=HisatomiMiki
en-aut-sei=Hisatomi
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=YanagiYoshinobu
en-aut-sei=Yanagi
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=AsaumiJunichi
en-aut-sei=Asaumi
en-aut-mei=Junichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Radiological Technology, Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Interdisciplinary Sciences and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Oral Radiology, Faculty of Dentistry, Hasanuddin University
kn-affil=

affil-num=12
en-affil=Department of Dentistry and Dental Surgery, College of Medicine and Health Sciences, An-Najah National University
kn-affil=

affil-num=13
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Oral Rehabilitation and Regenerative Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=16
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=17
en-affil=Department of Oral and Maxillofacial Radiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=head and neck tumors
kn-keyword=head and neck tumors
en-keyword=mean kurtosis
kn-keyword=mean kurtosis
en-keyword=simple diffusion kurtosis imaging
kn-keyword=simple diffusion kurtosis imaging
en-keyword=magnetic resonance imaging
kn-keyword=magnetic resonance imaging
en-keyword=apparent diffusion coefficient value
kn-keyword=apparent diffusion coefficient value
en-keyword=diffusion kurtosis imaging
kn-keyword=diffusion kurtosis imaging
en-keyword=machine learning
kn-keyword=machine learning
en-keyword=bi-parameter analysis
kn-keyword=bi-parameter analysis
en-keyword=gradient boosting
kn-keyword=gradient boosting
en-keyword=differential diagnosis of benign and malignant
kn-keyword=differential diagnosis of benign and malignant
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=
article-no=
start-page=1551700
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250305
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Acetoacetate, a ketone body, attenuates neuronal bursts in acutely-induced epileptiform slices of the mouse hippocampus
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The ketogenic diet increases ketone bodies (beta-hydroxybutyrate and acetoacetate) in the brain, and ameliorates epileptic seizures in vivo. However, ketone bodies exert weak or no effects on electrical activity in rodent hippocampal slices. Especially, it remains unclear what kinds of conditions are required to strengthen the actions of ketone bodies in hippocampal slices. In the present study, we examined the effects of acetoacetate on hippocampal pyramidal cells in normal slices and epileptiform slices of mice. By using patch-clamp recordings from CA1 pyramidal cells, we first confirmed that acetoacetate did not change the membrane potentials and intrinsic properties of pyramidal cells in normal slices. However, we found that acetoacetate weakened spontaneous epileptiform bursts in pyramidal cells of epileptiform slices, which were acutely induced by applying convulsants to normal slices. Interestingly, acetoacetate did not change the frequency of the epileptiform bursts, but attenuated individual epileptiform bursts. We finally examined the effects of acetoacetate on excitatory synaptic barrages during epileptiform activity, and found that acetoacetate weakened epileptiform bursts by reducing synchronous synaptic inputs. These results show that acetoacetate attenuated neuronal bursts in epileptiform slices, but did not affect neuronal activity in normal slices, which leads to seizure-selective actions of ketone bodies.
en-copyright=
kn-copyright=

en-aut-name=WenHao
en-aut-sei=Wen
en-aut-mei=Hao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SadaNagisa
en-aut-sei=Sada
en-aut-mei=Nagisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=InoueTsuyoshi
en-aut-sei=Inoue
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Biophysical Chemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biophysical Chemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Biophysical Chemistry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=epilepsy
kn-keyword=epilepsy
en-keyword=ketone body
kn-keyword=ketone body
en-keyword=ketogenic diet
kn-keyword=ketogenic diet
en-keyword=hippocampus
kn-keyword=hippocampus
en-keyword=slice physiology
kn-keyword=slice physiology
en-keyword=patch-clamp recording
kn-keyword=patch-clamp recording
END

start-ver=1.4
cd-journal=joma
no-vol=16
cd-vols=
no-issue=1
article-no=
start-page=1757
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250224
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Keratinocyte-driven dermal collagen formation in the axolotl skin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Type I collagen is a major component of the dermis and is formed by dermal fibroblasts. The development of dermal collagen structures has not been fully elucidated despite the major presence and importance of the dermis. This lack of understanding is due in part to the opacity of mammalian skin and it has been an obstacle to cosmetic and medical developments. We reveal the process of dermal collagen formation using the highly transparent skin of the axolotl and fluorescent collagen probes. We clarify that epidermal cells, not dermal fibroblasts, contribute to dermal collagen formation. Mesenchymal cells (fibroblasts) play a role in modifying the collagen fibers already built by keratinocytes. We confirm that collagen production by keratinocytes is a widely conserved mechanism in other model organisms. Our findings warrant a change in the current consensus about dermal collagen formation and could lead to innovations in cosmetology and skin medication.
en-copyright=
kn-copyright=

en-aut-name=OhashiAyaka
en-aut-sei=Ohashi
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KurodaJunpei
en-aut-sei=Kuroda
en-aut-mei=Junpei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KondoYohei
en-aut-sei=Kondo
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KameiYasuhiro
en-aut-sei=Kamei
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NonakaShigenori
en-aut-sei=Nonaka
en-aut-mei=Shigenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FurukawaSaya
en-aut-sei=Furukawa
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoSakiya
en-aut-sei=Yamamoto
en-aut-mei=Sakiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatohAkira
en-aut-sei=Satoh
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Frontier Biosciences, Osaka University
kn-affil=

affil-num=4
en-affil=Center for One Medicine Innovative Translational Research (COMIT), Nagoya University
kn-affil=

affil-num=5
en-affil=Laboratory for Biothermology, National Institute for Basic Biology
kn-affil=

affil-num=6
en-affil=The Graduate University for Advanced Studies (SOKENDAI)
kn-affil=

affil-num=7
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Environment, Life, Natural Science and Technology, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=7506
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250303
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A glucocorticoid-regulating molecule, Fkbp5, may interact with mitogen-activated protein kinase signaling in the organ of Corti of mice cochleae
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=FKBP5 is a 51-Da FK506-binding protein and member of the immunophilin family involved in controlling the signaling of glucocorticoid receptor from the cytosol to nucleus. Fkbp5 has previously been shown to be expressed in murine cochlear tissue, including the organ of Corti (i.e., the sensory epithelium of the cochlea). Fkbp5-/- mice as used in this study show hearing loss in the low-frequency (8-kHz) range and click-evoked auditory brainstem response (ABR) threshold compared to wild-type mice. Both Fkbp5-/- and wild-type mice showed hearing loss at all frequencies and click-ABR thresholds at 24 h and 14 days following acoustic overexposure (AO). Tissues of the organ of Corti were subjected to RNA sequencing and KEGG pathway analysis. In Fkbp5-/- mice before AO, the mitogen-activated protein kinase (MAPK) signaling pathway was dysregulated compared to wild-type mice. In wild-type mice at 12 h following AO, the most significantly modulated KEGG pathway was the TNF signaling pathway and major MAPK molecules p38 and Jun were involved in the TNF signaling pathway. In Fkbp5-/- mice at 12 h following AO, the MAPK signaling pathway was dysregulated compared to wild-type mice following AO. In conclusion, Fkbp5 interacts with MAPK signaling in the organ of Corti in mice cochleae.
en-copyright=
kn-copyright=

en-aut-name=SatoAsuka
en-aut-sei=Sato
en-aut-mei=Asuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OmichiRyotaro
en-aut-sei=Omichi
en-aut-mei=Ryotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaYukihide
en-aut-sei=Maeda
en-aut-mei=Yukihide
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AndoMizuo
en-aut-sei=Ando
en-aut-mei=Mizuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Otolaryngology-Head and Neck Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=The organ of Corti
kn-keyword=The organ of Corti
en-keyword=Acoustic trauma
kn-keyword=Acoustic trauma
en-keyword=RNA sequencing
kn-keyword=RNA sequencing
en-keyword=51-Da FK506-binding protein
kn-keyword=51-Da FK506-binding protein
en-keyword=Mitogen-activated protein kinase signaling
kn-keyword=Mitogen-activated protein kinase signaling
en-keyword=Tumor necrosis factor signaling
kn-keyword=Tumor necrosis factor signaling
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=4
article-no=
start-page=1391
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250219
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Course of General Fatigue in Patients with Post-COVID-19 Conditions Who Were Prescribed Hochuekkito: A Single-Center Exploratory Pilot Study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: After the start of the COVID-19 pandemic, general fatigue in patients with long COVID and post-COVID-19 conditions (PCC) became a medical issue. Although there is a lack of evidence-based treatments, Kampo medicine (traditional Japanese medicine) has gained attention in Japan. At an outpatient clinic in Japan specializing in long COVID, 24% of all prescriptions were Kampo medicines, and 72% of Kampo medicine prescriptions were hochuekkito. However, there has been no prospective, quantitative study on the course of fatigue in patients with long COVID and PCC who were prescribed hochuekkito. The aim of this study was to clarify the course of fatigue in those patients. Methods: This study included patients aged 18 years or older with general fatigue who visited the long COVID specialized outpatient clinic at Okayama University Hospital and consented to participate after being prescribed hochuekkito. We reviewed the backgrounds of the patients, and we evaluated the patients' fatigue assessment scale in person or online. Results: Twenty patients were enrolled in this study from September to December in 2023. The average age of the patients was 42.9 years (SD: 15.8 years) and 12 patients (60%) were female. After hochuekkito administration, the fatigue assessment scale score decreased from 35.9 (SD: 5.9) at the initial visit to 31.2 (SD: 9.4) after 8 weeks, indicating a trend for improvement in fatigue (difference: 4.7; 95% CI: 0.5-8.9). Conclusions: A trend for improvement in fatigue was observed in patients with long COVID and PCC who were prescribed hochuekkito, indicating a potential benefit of hochuekkito for general fatigue in such patients. General fatigue in patients with long COVID or PCC can be classified as post-infectious fatigue syndrome and is considered a condition of qi deficiency in Kampo medicine, for which hochuekkito is appropriately indicated.
en-copyright=
kn-copyright=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsukiNobuyoshi
en-aut-sei=Matsuki
en-aut-mei=Nobuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SakamotoYoko
en-aut-sei=Sakamoto
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=fatigue assessment scale (FAS)
kn-keyword=fatigue assessment scale (FAS)
en-keyword= general fatigue
kn-keyword= general fatigue
en-keyword= hochuekkito
kn-keyword= hochuekkito
en-keyword= kampo medicine
kn-keyword= kampo medicine
en-keyword= long COVID
kn-keyword= long COVID
en-keyword= post-COVID-19 condition
kn-keyword= post-COVID-19 condition
END

start-ver=1.4
cd-journal=joma
no-vol=197
cd-vols=
no-issue=
article-no=
start-page=115301
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202503
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Fraglide-1 from traditional Chinese aromatic vinegar: A natural AhR antagonist for atopic dermatitis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Traditional Chinese Zhenjiang aromatic vinegar (Kozu) contains Fraglide-1 (FG1), a bioactive lactone with demonstrated peroxisome proliferator-activated receptor gamma (PPAR��) agonist and antioxidant activities. This study explored FG1's novel ability to antagonize the aryl hydrocarbon receptor (AhR) signaling pathway, which regulates artemin expression and contributes to itching and inflammation in atopic dermatitis. Through molecular docking simulations and cell-based assays in human keratinocytes, we demonstrated FG1's potent antagonistic activity against AhR signaling. FG1 effectively suppressed FICZ-induced inflammatory responses, including artemin expression, with potency (half maximal inhibitory concentration, IC50 = 5.1 ��M) comparable to the synthetic antagonist StemRegenin 1 (SR1) while demonstrating a superior safety profile (median lethal concentration, LC50 > 100 ��M vs. 27.5 ��M for SR1). These findings expand our understanding of bioactive compounds from traditional fermented foods and their regulatory effects on AhR signaling, providing a foundation for future studies on FG1's role in modulating skin inflammation.
en-copyright=
kn-copyright=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AkamatsuMiki
en-aut-sei=Akamatsu
en-aut-mei=Miki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KakimaruSaya
en-aut-sei=Kakimaru
en-aut-mei=Saya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakagiMasahiro
en-aut-sei=Takagi
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyashitaMasahiro
en-aut-sei=Miyashita
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=School of Materials Science, Japan Advanced Institute of Science and Technology
kn-affil=

affil-num=6
en-affil=Graduate School of Agriculture, Kyoto University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=9
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Graduate School of Science, Technology and Innovation, Kobe University
kn-affil=
en-keyword=AhR
kn-keyword=AhR
en-keyword=Xenobiotic responsive element
kn-keyword=Xenobiotic responsive element
en-keyword=StemRegenin 1
kn-keyword=StemRegenin 1
en-keyword=ARNT
kn-keyword=ARNT
en-keyword=Atopic dermatitis
kn-keyword=Atopic dermatitis
en-keyword=Artemin
kn-keyword=Artemin
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Spatiotemporal expression pattern of dyslexia susceptibility 1 candidate 1 (DYX1C1) during rat cerebral cortex development
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Developmental dyslexia (DD) is a common learning disorder with significant consequences for affected individuals. Although several candidate genes, including dyslexia susceptibility 1 candidate 1 (DYX1C1), have been implicated in dyslexia, their role in brain development remains unclear. We aimed to elucidate the spatiotemporal expression patterns of DYX1C1 during cerebral cortex development in rats.<br>
Methods We investigated DYX1C1 expression during cerebral cortex development using rat embryos at various gestational stages (E13.5, 15.5, 17.5 and 20.5) by immunohistochemistry (n?=?7 embryos/stage), quantitative real-time PCR (n?=?6), and in situ hybridization (n?=?11?15).<br>
Results The DYX1C1-positive cells were predominantly located in the outermost layers of the cortical plate, particularly at E15.5. DYX1C1 mRNA expression peaked at E15.5 and subsequently declined. DYX1C1-positive cells did not co-localize with reelin-positive Cajal-Retzius cells, but co-localized with neuronal markers expressed during development, and had shorter primary cilia than DYX1C1-negative cells.<br>
Conclusions Our findings highlight the dynamic expression of DYX1C1 in the developing cerebral cortex of rats, implicating its involvement in neurodevelopmental processes. Further investigation of the functional interactions of DYX1C1, particularly its relationship with reelin and its role in cerebrocortical and hippocampal development, may provide insights into the pathophysiology of dyslexia and neurodevelopmental disorders.
en-copyright=
kn-copyright=

en-aut-name=ZenshoKazumasa
en-aut-sei=Zensho
en-aut-mei=Kazumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IsseAika
en-aut-sei=Isse
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MisawaIchika
en-aut-sei=Misawa
en-aut-mei=Ichika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OkaMakio
en-aut-sei=Oka
en-aut-mei=Makio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Psychosocial Medicine, National Center for Child Health and Development
kn-affil=

affil-num=7
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=79
cd-vols=
no-issue=1
article-no=
start-page=1
end-page=7
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=202502
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Endothelial Cell Polarity in Health and Disease
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Endothelial cell polarity is fundamental to the organization and function of blood vessels, influencing processes such as angiogenesis, vascular stability, and response to shear stress. This review elaborates on the molecular mechanisms that regulate endothelial cell polarity, focusing on key players like the PAR polarity complex and Rho family GTPases. These pathways coordinate the front?rear, apical?basal and planar polarity of endothelial cells, which are essential for the proper formation and maintenance of vascular structures. In health, endothelial polarity ensures not only the orderly development of blood vessels, with tip cells adopting distinct polarities during angiogenesis, but also ensures proper vascular integrity and function. In disease states, however, disruptions in polarity contribute to pathologies such as coronary artery disease, where altered planar polarity exacerbates atherosclerosis, and cancer, where disrupted polarity in tumor vasculature leads to abnormal vessel growth and function. Understanding cell polarity and its disruption is fundamental not only to comprehending how cells interact with their microenvironment and organize themselves into complex, organ-specific tissues but also to developing novel, targeted, and therapeutic strategies for a range of diseases, from cardiovascular disorders to malignancies, ultimately improving patient outcomes.
en-copyright=
kn-copyright=

en-aut-name=ThihaMoe
en-aut-sei=Thiha
en-aut-mei=Moe
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HikitaTakao
en-aut-sei=Hikita
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakayamaMasanori
en-aut-sei=Nakayama
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pathophysiology and Drug Discovery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=blood vessel
kn-keyword=blood vessel
en-keyword=endothelial cell
kn-keyword=endothelial cell
en-keyword=cell polarity
kn-keyword=cell polarity
en-keyword=atherosclerosis
kn-keyword=atherosclerosis
en-keyword=cancer
kn-keyword=cancer
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=���\���E�p���ڎ�
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=
article-no=
start-page=27
end-page=38
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The List of Published by Members of the Faculty From January to December 2024.
kn-title=���\�w�p�_�������X�g�@2024
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=114
cd-vols=
no-issue=
article-no=
start-page=11
end-page=20
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Uncovering the role of arcuate kisspeptin neurons as a source of the gonadotropin-releasing hormone pulse generator using gene-modified rats
kn-title=��`�q���σ��b�g��p�����|��j�L�X�y�v�`���j���[�����̐��B�h���z���������o�z�������p���X�W�F�l���[�^�[�Ƃ��Ă̖�����
en-subtitle=
kn-subtitle=
en-abstract=�@���E�ɂ����āC�����̎�ٗ��i�D�P���j���ቺ���Ă���C�ƒ{�̔ɐB���ь���̂��߂̌��ʓI�Ȏ��Ö@���K�v�Ƃ���Ă���D�ƒ{���܂ޚM���ނɂ����āC���B�@�\�͎��������|�����́|���B�����番�傳���z�������ɂ���Đ��䂳��Ă���D�����̃z�������̂����C���B�h���z���������o�z�������iGnRH�j�̃p���X�󕪔�iGnRH �p���X�j�́C���B�h���z����������Ɛ��B�@�\�ɖ{���I�ɏd�v�ł���D���������āCGnRH �p���X�𐧌䂷�郁�J�j�Y���iGnRH �p���X�W�F�l���[�^�[�j���𖾂��邱�Ƃ́C�ƒ{�̐��B�Z�p�����コ���邽�߂ɕs���ł���D�{�����ł́C���҂�̈�`�q���σ��b�g���f����p�����|��j�L�X�y�v�`���j���[�����i��NDy �j���[�����Ƃ��Ă��m����j��GnRH �p���X�W�F�l���[�^�[�̖{�̂ł��邱�Ƃ̒��ړI�ȏ؋��������������𒆐S�Ƃ��āC�ߋ�20�N�Ԃ̌������T�������D�܂��C��NDy �j���[���������傷��j���[���L�j��B�C�O���^�~���_�C�_�C�m���t�B��A ����NDy �j���[�����̐_�o�����𓯊������CGnRH �p���X�𔭐������郁�J�j�Y���ɂ��Ę_�����D��`�q���σ��b�g���f�����瓾��ꂽ�m���́CGnRH/ ���B�h���z�������p���X���h�����āC�ƒ{�̔ɐB�\�͂����コ����V�K�ɐB���i�܊J���Ɋ�^����Ɗ��҂ł���D
kn-abstract=�@Strategies for increasing reproductive performance are needed for domestic animals because for example the conception (pregnancy) rate has decreased in dairy cows around the world. Reproductive function is controlled by hormones released by the hypothalamus-pituitary-gonadal axis in mammals, including domestic animals. Of those hormones, tonic (pulsatile) gonadotropin-releasing hormone (GnRH) release is fundamentally important for gonadotropin release and gonadal activity. Therefore, uncovering the mechanism controlling GnRH pulses, that is GnRH pulse generator, is essential to improve reproductive technologies for domestic animals. The present review is focused on the indispensable role of arcuate nucleus (ARC) kisspeptin neurons (also known as KNDy neurons) as the GnRH pulse generator in mammals. First, we give a brief overview of studies on hypothalamic kisspeptin neurons throughout the past two decades. Second, we review studies that have provided direct evidence that ARC kisspeptin neurons serve as the GnRH pulse generator, with a special focus on our gene-modified rat models. Finally, we discuss the mechanism underlying GnRH pulse generation. The knowledge obtained from gene-modified rat models should be clinically important and could be adapted to new tools to improve reproductive performance in livestock by stimulating GnRH/gonadotropin pulses.
en-copyright=
kn-copyright=

en-aut-name=NagaeMayuko
en-aut-sei=Nagae
en-aut-mei=Mayuko
kn-aut-name=���]���C�q
kn-aut-sei=���]
kn-aut-mei=���C�q
aut-affil-num=1
ORCID=

en-aut-name=UenoyamaYoshihisa
en-aut-sei=Uenoyama
en-aut-mei=Yoshihisa
kn-aut-name=���R��v
kn-aut-sei=���R
kn-aut-mei=��v
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=���R��w��w�@���������R�Ȋw������

affil-num=2
en-affil=Graduate School of Bioagricultural Sciences, Nagoya University
kn-affil=���É���w��w�@�����_�w������
en-keyword=gene-modified rats
kn-keyword=gene-modified rats
en-keyword=GnRH
kn-keyword=GnRH
en-keyword=kisspeptin
kn-keyword=kisspeptin
en-keyword=LH
kn-keyword=LH
en-keyword=pulse generator
kn-keyword=pulse generator
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=63
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250113
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Impact of Task Context on Pleasantness and Softness Estimations: A Study Based on Three Touch Strategies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This study investigated the two distinct perceptions (pleasantness and softness) of deformable stimuli with different degrees of compliance under conditions with and without a contextual task. Three tactile strategies-grasping, pinching, and pressing-were used to perceive the stimuli. In Experiment 1 (without a contextual task), participants estimated the perceived intensity of softness or pleasantness for each stimulus. In Experiment 2 (with a contextual task), the participants sequentially perceived two stimuli with different compliance levels and indicated which stimulus they perceived as softer and pleasant. The results showed that the psychophysical relationship between compliance and perceived softness was consistent across all tactile strategies in both experiments, with softness estimates increasing as compliance increased. However, the relationship between compliance and pleasantness differed between the two experiments. In Experiment 1, pleasantness estimates increased monotonically with increased compliance. However, in Experiment 2, across all tactile strategies, pleasantness began to decrease within the compliance range of 0.25-2.0 cm2/N, exhibiting an inverted U-shaped trend. These findings indicate that the relationship between compliance and pleasantness is task-dependent, particularly demonstrating significantly different trends when a contextual task is introduced. In contrast, the relationship between compliance and softness remained consistently monotonic.
en-copyright=
kn-copyright=

en-aut-name=GaoBinyue
en-aut-sei=Gao
en-aut-mei=Binyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=EjimaYoshimichi
en-aut-sei=Ejima
en-aut-mei=Yoshimichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WuJinglong
en-aut-sei=Wu
en-aut-mei=Jinglong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=pleasantness
kn-keyword=pleasantness
en-keyword=softness
kn-keyword=softness
en-keyword=touch strategy
kn-keyword=touch strategy
en-keyword=task context
kn-keyword=task context
en-keyword=psychophysics
kn-keyword=psychophysics
END

start-ver=1.4
cd-journal=joma
no-vol=43
cd-vols=
no-issue=1
article-no=
start-page=4
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2025
dt-pub=20250114
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To identify factors involved in methamphetamine (METH) neurotoxicity, we comprehensively searched for genes which were differentially expressed in mouse striatum after METH administration using differential display (DD) reverse transcription-PCR method and sequent single-strand conformation polymorphism analysis, and found two DD cDNA fragments later identified as mRNA of Nedd4 (neural precursor cell expressed developmentally downregulated 4) WW domain-binding protein 5 (N4WBP5), later named Nedd4 family-interacting protein 1 (Ndfip1). It is an adaptor protein for the binding between Nedd4 of ubiquitin ligase (E3) and target substrate protein for ubiquitination. Northern blot analysis confirmed drastic increases in Ndfip1 mRNA in the striatum after METH injections, and in situ hybridization histochemistry showed that the mRNA expression was increased in the hippocampus and cerebellum at 2 h-2 days, in the cerebral cortex and striatum at 18 h-2 days after single METH administration. The knockdown of Ndfip1 expression with Ndfip1 siRNA significantly aggravated METH-induced neurotoxicity in the cultured monoaminergic neuronal cells. These results suggest that drastic increases in Ndfip1 mRNA is compensatory reaction to protect neurons against METH-induced neurotoxicity.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=CadetJean Lud
en-aut-sei=Cadet
en-aut-mei=Jean Lud
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Molecular Neuropsychiatry Section, Intramural Research Program, NIH/ NIDA
kn-affil=
en-keyword=Methamphetamine
kn-keyword=Methamphetamine
en-keyword=Neurotoxicity
kn-keyword=Neurotoxicity
en-keyword=Nedd4
kn-keyword=Nedd4
en-keyword=Ndfip1
kn-keyword=Ndfip1
en-keyword=Differential display
kn-keyword=Differential display
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=2
article-no=
start-page=125
end-page=132
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202412
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=�i�g���E���`���l���ُ�ƂĂ񂩂�
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=���i�����j�ɐD
kn-aut-sei=���i�����j
kn-aut-mei=�ɐD
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=���R��w�w�p�����@����w��
END

start-ver=1.4
cd-journal=joma
no-vol=326
cd-vols=
no-issue=6
article-no=
start-page=F1054
end-page=F1065
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240530
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Diabetic nephropathy remains the leading cause of end-stage kidney disease in many countries, and additional therapeutic targets are needed to prevent its development and progression. Some angiogenic factors are involved in the pathogenesis of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel proangiogenic factor, and our previous study showed that glomerular damage is inhibited in diabetic Vash2 homozygous knockout mice. Therefore, we established a VASH2-targeting peptide vaccine as a tool for anti-VASH2 therapy in diabetic nephropathy. In this study, the preventive effects of the VASH2-targeting peptide vaccine against glomerular injury were examined in a streptozotocin (STZ)-induced diabetic mouse model. The mice were subcutaneously injected with the vaccine at two doses 2 wk apart and then intraperitoneally injected with 50 mg/kg STZ for 5 consecutive days. Glomerular injury was evaluated 20 wk after the first vaccination. Treatment with the VASH2-targeting peptide vaccine successfully induced circulating anti-VASH2 antibody without inflammation in major organs. Although the vaccination did not affect blood glucose levels, it significantly prevented hyperglycemia-induced increases in urinary albumin excretion and glomerular volume. The vaccination did not affect increased VASH2 expression but significantly inhibited renal angiopoietin-2 (Angpt2) expression in the diabetic mice. Furthermore, it significantly prevented glomerular macrophage infiltration. The preventive effects of vaccination on glomerular injury were also confirmed in db/db mice. Taken together, the results of this study suggest that the VASH2-targeting peptide vaccine may prevent diabetic glomerular injury in mice by inhibiting Angpt2-mediated microinflammation.
en-copyright=
kn-copyright=

en-aut-name=NakashimaYuri
en-aut-sei=Nakashima
en-aut-mei=Yuri
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanabeKatsuyuki
en-aut-sei=Tanabe
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MifuneTomoyo
en-aut-sei=Mifune
en-aut-mei=Tomoyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakadoiTakato
en-aut-sei=Nakadoi
en-aut-mei=Takato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HayashiHiroki
en-aut-sei=Hayashi
en-aut-mei=Hiroki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakagamiHironori
en-aut-sei=Nakagami
en-aut-mei=Hironori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SatoYasufumi
en-aut-sei=Sato
en-aut-mei=Yasufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Health Development and Medicine, Osaka University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=New Industry Creation Hatchery Center, Tohoku University
kn-affil=

affil-num=8
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=albuminuria
kn-keyword=albuminuria
en-keyword=diabetic nephropathy
kn-keyword=diabetic nephropathy
en-keyword=macrophages
kn-keyword=macrophages
en-keyword=peptide vaccine
kn-keyword=peptide vaccine
en-keyword=vasohibin-2
kn-keyword=vasohibin-2
END

start-ver=1.4
cd-journal=joma
no-vol=169
cd-vols=
no-issue=1
article-no=
start-page=e16291
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241222
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Exploring the Role of Ccn3 in Type III Cell of Mice Taste Buds
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Different taste cells express unique cell-type markers, enabling researchers to distinguish them and study their functional differentiation. Using single-cell RNA-Seq of taste cells in mouse fungiform papillae, we found that Cellular Communication Network Factor 3 (Ccn3) was highly expressed in Type III taste cells but not in Type II taste cells. Ccn3 is a protein-coding gene involved in various biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Therefore, in this study, we aimed to explore the expression and function of Ccn3 in mouse taste bud cells. Using reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemistry (IHC), we confirmed that Ccn3 was predominantly expressed in Type III taste cells. Through IHC, quantitative real-time RT-PCR, gustatory nerve recordings, and short-term lick tests, we observed that Ccn3 knockout (Ccn3-KO) mice did not exhibit any significant differences in the expression of taste cell markers and taste responses compared to wild-type controls. To explore the function of Ccn3 in taste cells, bioinformatics analyses were conducted and predicted possible roles of Ccn3 in tissue regeneration, perception of pain, protein secretion, and immune response. Among them, an immune function is the most plausible based on our experimental results. In summary, our study indicates that although Ccn3 is strongly expressed in Type III taste cells, its knockout did not influence the basic taste response, but bioinformatics provided valuable insights into the possible role of Ccn3 in taste buds and shed light on future research directions.
en-copyright=
kn-copyright=

en-aut-name=WangKuanyu
en-aut-sei=Wang
en-aut-mei=Kuanyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=bioinformatics
kn-keyword=bioinformatics
en-keyword=Ccn3
kn-keyword=Ccn3
en-keyword=Type III taste cell
kn-keyword=Type III taste cell
END

start-ver=1.4
cd-journal=joma
no-vol=17
cd-vols=
no-issue=3-4
article-no=
start-page=116
end-page=125
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Deep Reinforcement Learning Enabled Adaptive Virtual Machine Migration Control in Multi-Stage Information Processing Systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper tackles a Virtual Machine (VM) migration control problem to maximize the progress (accuracy) of information processing tasks in multi-stage information processing systems. The conventional methods for this problem are effective only for specific situations, such as when the system load is high. In this paper, in order to adaptively achieve high accuracy in various situations, we propose a VM migration method using a Deep Reinforcement Learning (DRL) algorithm. It is difficult to directly apply a DRL algorithm to the VM migration control problem because the size of the solution space of the problem dynamically changes according to the number of VMs staying in the system while the size of the agent�fs action space is fixed in DRL algorithms. To cope with this difficulty, the proposed method divides the VM migration control problem into two problems: the problem of determining only the VM distribution (i.e., the proportion of the number of VMs deployed on each edge server) and the problem of determining the locations of all the VMs so that it follows the determined VM distribution. The former problem is solved by a DRL algorithm, and the latter by a heuristic method. This approach makes it possible to apply a DRL algorithm to the VM migration control problem because the VM distribution is expressed by a vector with a fixed number of dimensions and can be directly outputted by the agent. The simulation results confirm that our proposed method can adaptively achieve quasi-optimal accuracy in various situations with different link delays, types of the information processing tasks and the number of VMs.
en-copyright=
kn-copyright=

en-aut-name=FukushimaYukinobu
en-aut-sei=Fukushima
en-aut-mei=Yukinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoujitaniYuki
en-aut-sei=Koujitani
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakaneKazutoshi
en-aut-sei=Nakane
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TarutaniYuya
en-aut-sei=Tarutani
en-aut-mei=Yuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WuCelimuge
en-aut-sei=Wu
en-aut-mei=Celimuge
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JiYusheng
en-aut-sei=Ji
en-aut-mei=Yusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YokohiraTokumi
en-aut-sei=Yokohira
en-aut-mei=Tokumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MuraseTutomu
en-aut-sei=Murase
en-aut-mei=Tutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Information Science Nagoya University
kn-affil=

affil-num=4
en-affil=Graduate School of Engineering Osaka University
kn-affil=

affil-num=5
en-affil=Graduate School of Informatics and Engineering The Univ. of Electro-Commun.
kn-affil=

affil-num=6
en-affil=Information Systems Architecture Research Division National Institute of Informatics
kn-affil=

affil-num=7
en-affil=Faculty of Interdisciplinary Science and Engineering in Health Systems Okayama University
kn-affil=

affil-num=8
en-affil=Graduate School of Information Science Nagoya University
kn-affil=
en-keyword=Multi-stage information processing system
kn-keyword=Multi-stage information processing system
en-keyword=VM migration control
kn-keyword=VM migration control
en-keyword=Deep reinforcement learning
kn-keyword=Deep reinforcement learning
en-keyword=Deep Deterministic Policy Gradient (DDPG)
kn-keyword=Deep Deterministic Policy Gradient (DDPG)
END

start-ver=1.4
cd-journal=joma
no-vol=18
cd-vols=
no-issue=3
article-no=
start-page=769
end-page=774
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230519
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Review: Nicotinic acetylcholine receptors to regulate important brain activity?what occurs at the molecular level?
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Herein, we briefly review the role of nicotinic acetylcholine receptors in regulating important brain activity by controlled release of acetylcholine from subcortical neuron groups, focusing on a microscopic viewpoint and considering the nonlinear dynamics of biological macromolecules associated with neuron activity and how they give rise to advanced brain functions of brain.
en-copyright=
kn-copyright=

en-aut-name=NaraShigetoshi
en-aut-sei=Nara
en-aut-mei=Shigetoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamagutiYutaka
en-aut-sei=Yamaguti
en-aut-mei=Yutaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsudaIchiro
en-aut-sei=Tsuda
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Information Engineering, Fukuoka Institute of Technology
kn-affil=

affil-num=3
en-affil=Chubu University Academy of Emerging Sciences/Center for Mathematical Science and Artificial Intelligence, Chubu University
kn-affil=
en-keyword=Neuromodulator
kn-keyword=Neuromodulator
en-keyword=Nichotinic
kn-keyword=Nichotinic
en-keyword=Acetylcholine
kn-keyword=Acetylcholine
en-keyword=Receptors
kn-keyword=Receptors
en-keyword=Brain activity
kn-keyword=Brain activity
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=12
article-no=
start-page=e0315385
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241209
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phase-dependent trends in the prevalence of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) related to long COVID: A criteria-based retrospective study in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background <br>
The characteristics of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) related to COVID-19 have remained uncertain. To elucidate the clinical trend of ME/CFS induced by long COVID, we examined data for patients who visited our outpatient clinic established in a university hospital during the period from Feb 2021 to July 2023.<br>
<br>
Methods <br>
Long COVID patients were classified into two groups, an ME/CFS group and a non-ME/CFS group, based on three diagnostic criteria.<br>
<br>
Results <br>
The prevalence of ME/CFS in the long COVID patients was 8.4% (62 of 739 cases; female: 51.6%) and factors related to ME/CFS were severe illness, smoking and alcohol drinking habits, and fewer vaccinations. The frequency of ME/CFS decreased from 23.9% in the Preceding period to 13.7% in the Delta-dominant period and to 3.3% in the Omicron-dominant period. Fatigue and headache were commonly frequent complaints in the ME/CFS group, and the frequency of poor concentration in the ME/CFS group was higher in the Omicron period. Serum ferritin levels were significantly higher in female patients in the ME/CFS group infected in the Preceding period. In the ME/CFS group, the proportion of patients complaining of brain fog significantly increased from 22.2% in the Preceding period to 47.9% in the Delta period and to 81.3% in the Omicron period. The percentage of patients who had received vaccination was lower in the ME/CFS group than the non-ME/CFS group over the study period, whereas there were no differences in the vaccination rate between the groups in each period.<br>
<br>
Conclusion <br>
The proportion of long COVID patients who developed ME/CFS strictly diagnosed by three criteria was lower among patients infected in the Omicron phase than among patients infected in the other phases, while the proportion of patients with brain fog inversely increased. Attention should be paid to the variant-dependent trends of ME/CFS triggered by long COVID (300 words).
en-copyright=
kn-copyright=

en-aut-name=MoritaSatoru
en-aut-sei=Morita
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=
article-no=
start-page=1468230
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241206
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Perspectives of traditional herbal medicines in treating retinitis pigmentosa
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Medicinal plants, also known as herbs, have been discovered and utilized in traditional medical practice since prehistoric times. Medicinal plants have been proven rich in thousands of natural products that hold great potential for the development of new drugs. Previously, we reviewed the types of Chinese traditional medicines that a Tang Dynasty monk Jianzhen (Japanese: Ganjin) brought to Japan from China in 742. This article aims to review the origin of Kampo (Japanese traditional medicine), and to present the overview of neurodegenerative diseases and retinitis pigmentosa as well as medicinal plants in some depth. Through the study of medical history of the origin of Kampo, we found that herbs medicines contain many neuroprotective ingredients. It provides us a new perspective on extracting neuroprotective components from herbs medicines to treat neurodegenerative diseases. Retinitis pigmentosa (one of the ophthalmic neurodegenerative diseases) is an incurable blinding disease and has become a popular research direction in global ophthalmology. To date, treatments for retinitis pigmentosa are very limited worldwide. Therefore, we intend to integrate the knowledge and skills from different disciplines, such as medical science, pharmaceutical science and plant science, to take a new therapeutic approach to treat neurodegenerative diseases. In the future, we will use specific active ingredients extracted from medicinal plants to treat retinitis pigmentosa. By exploring the potent bioactive ingredients present in medicinal plants, a valuable opportunity will be offered to uncover novel approaches for the development of drugs which target for retinitis pigmentosa.
en-copyright=
kn-copyright=

en-aut-name=LiuShihui
en-aut-sei=Liu
en-aut-mei=Shihui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsuoChie
en-aut-sei=Matsuo
en-aut-mei=Chie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=AbeTakumi
en-aut-sei=Abe
en-aut-mei=Takumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ChenJinghua
en-aut-sei=Chen
en-aut-mei=Jinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunChi
en-aut-sei=Sun
en-aut-mei=Chi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ZhaoQing
en-aut-sei=Zhao
en-aut-mei=Qing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Ophthalmology, University of Florida, College of Medicine
kn-affil=

affil-num=6
en-affil=Department of Ophthalmology and Visual Sciences, Washington University in St. Louis
kn-affil=

affil-num=7
en-affil=National Key Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences
kn-affil=
en-keyword=retinitis pigmentosa
kn-keyword=retinitis pigmentosa
en-keyword=ophthalmology
kn-keyword=ophthalmology
en-keyword=botany
kn-keyword=botany
en-keyword=pharmacology
kn-keyword=pharmacology
en-keyword=medical history
kn-keyword=medical history
en-keyword=compound
kn-keyword=compound
en-keyword=drug discovery
kn-keyword=drug discovery
en-keyword=degenerative diseases
kn-keyword=degenerative diseases
END

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dt-received=
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dt-pub-year=2024
dt-pub=20240925
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en-subject=
kn-subject=
en-title=���ۉ��𔺂��X����������̗��̔|�{�@�ɂ��V�Kin vitro���f���̍\�z�Ɖ��
kn-title=Establishment and Analysis of Novel In Vitro 3D Cell Culture Models of the Fibrotic Tumor Microenvironment in Pancreatic Cancer
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kn-subtitle=
en-abstract=
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kn-copyright=

en-aut-name=TANAKAHiroyoshi
en-aut-sei=TANAKA
en-aut-mei=Hiroyoshi
kn-aut-name=�c���[��
kn-aut-sei=�c��
kn-aut-mei=�[��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Okayama University
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dt-received=
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kn-title=Power suppression in EEG after the onset of SAH is a significant marker of early brain injury in rat models
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en-aut-name=TAKASUGIYuji
en-aut-sei=TAKASUGI
en-aut-mei=Yuji
kn-aut-name=�����S��
kn-aut-sei=����
kn-aut-mei=�S��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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END

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en-title=���ԗ\�����G�o�m�o�̌`���ɗ^����e���̐_�o��Ղ̉�
kn-title=The neural substrates of temporal prediction forming tactile perception in humans
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en-aut-name=RENRONGXIA
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kn-aut-sei=�C
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aut-affil-num=1
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affil-num=1
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en-title=��ϓI�F�m�@�\�̒ቺ�������o�����ƃN���X���[�_���g���[�j���O�ɗ^����e��
kn-title=Effects of Subjective Cognitive Decline on Audiovisual Integration and Cross-modal Training
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en-aut-name=LISHENGNAN
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kn-aut-name=������
kn-aut-sei=��
kn-aut-mei=����
aut-affil-num=1
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affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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en-title=Go/No-Go�ۑ��p�����^���}���̐_�o��Ղ̉�
kn-title=The neural substrates of motion inhibitory control during Go/No-Go response inhibition task
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kn-subtitle=
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en-aut-name=ZHANGNAN
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en-aut-mei=NAN
kn-aut-name=����
kn-aut-sei=��
kn-aut-mei=��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=���R��w��w�@�w���X�V�X�e�������Ȋw������
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en-title=�R���s���[�^�[�r�W�����ɂ��H���ێ�ʐ���Z�p
kn-title=Computer Vision Systems for Estimating Food Consumption in a Hospital Setting
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kn-subtitle=
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en-aut-name=YUITA ARUM SARI
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kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=���R��w��w�@�w���X�V�X�e�������Ȋw������
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en-title=�R���s���[�^�E�r�W�����ɂ�铮���̌��o�Z�p�Ɛ��q�i������ւ̉��p
kn-title=Computer Vision-based Motion Segmentation and Its Application for Sperm Quality Estimation
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kn-subtitle=
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en-aut-name=SIGIT ADINUGROHO
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kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=���R��w��w�@�w���X�V�X�e�������Ȋw������
END

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en-title=����זE�ւ�siRNA���B�̂��߂̃y�v�`�h�i�m�~�Z���̊J��
kn-title=Development of Peptide Nanomicelle for siRNA Delivery into Cancer Cells
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en-aut-name=TAUFIK FATWA NUR HAKIM
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kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=���R��w��w�@�w���X�V�X�e�������Ȋw������
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en-title=IoT�A�v���P�[�V�����E�V�X�e���̂��߂̓����T�[�o�E�v���b�g�t�H�[���Ɋւ��錤��
kn-title=A Study of Integrated Server Platform for IoT Application Systems
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kn-subtitle=
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en-aut-name=YOHANES YOHANIE FRIDELIN PANDUMAN
en-aut-sei=YOHANES YOHANIE FRIDELIN PANDUMAN
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
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en-aut-name=SEKIGUCHIManabu
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kn-aut-mei=�w
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ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
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kn-subject=
en-title=�����̐V�^�R���i�E�C���X�����ǜ늳��Ǐ�ɂ݂��錎�o�֘A�Ǐ�̌���
kn-title=Clinical characteristics of female long COVID patients with menstrual symptoms: a retrospective study from a Japanese outpatient clinic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SAKURADAYasue
en-aut-sei=SAKURADA
en-aut-mei=Yasue
kn-aut-name=�N�c�׍]
kn-aut-sei=�N�c
kn-aut-mei=�׍]
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=���������_�o���ᇂ̂��񊲍זE���ێ��ɑ΂���J�e�R���~�������y�f�̖���
kn-title=Role of catecholamine synthases in the maintenance of cancer stem-like cells in malignant peripheral nerve sheath tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KATAYAMAHaruyoshi
en-aut-sei=KATAYAMA
en-aut-mei=Haruyoshi
kn-aut-name=�ЎR����
kn-aut-sei=�ЎR
kn-aut-mei=����
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=�_���X�g���X�Ɖ��ǔ����Ɋւ���}�E�X�]�������f���ɂ�����J���m�V���̐_�o�ی����
kn-title=Neuroprotective effects of carnosine in a mice stroke model concerning oxidative stress and inflammatory response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HUXINRAN
en-aut-sei=HU
en-aut-mei=XINRAN
kn-aut-name=�Ӌәf
kn-aut-sei=��
kn-aut-mei=�әf
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=���������_�o���ᇂɂ�����PRRX1��TOP2A�̃^���p�N���ԑ��ݍ�p�͈������𑣐i������
kn-title=PRRX1-TOP2A interaction is a malignancy-promoting factor in human malignant peripheral nerve sheath tumours
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TAKIHIRAShota
en-aut-sei=TAKIHIRA
en-aut-mei=Shota
kn-aut-name=�畽����
kn-aut-sei=�畽
kn-aut-mei=����
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=2
article-no=
start-page=35
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230511
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of the Follow-Up Human 3D Oral Cancer Model in Cancer Treatment
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=As function preservation cancer therapy, targeted radiation therapies have been developed for the quality of life of cancer patients. However, preclinical animal studies evaluating the safety and efficacy of targeted radiation therapy is challenging from the viewpoints of animal welfare and animal protection, as well as the management of animal in radiation-controlled areas under the regulations. We fabricated the human 3D oral cancer model that considers the time axis of the follow up in cancer treatment. Therefore, in this study, the 3D model with human oral cancer cells and normal oral fibroblasts was treated based on clinical protocol. After cancer treatment, the histological findings of the 3D oral cancer model indicated the clinical correlation between tumor response and surrounding normal tissue. This 3D model has potential as a tool for preclinical studies alternative to animal studies.
en-copyright=
kn-copyright=

en-aut-name=IgawaKazuyo
en-aut-sei=Igawa
en-aut-mei=Kazuyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IzumiKenji
en-aut-sei=Izumi
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SakuraiYoshinori
en-aut-sei=Sakurai
en-aut-mei=Yoshinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Neutron Therapy Research Center, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Biomimetics, Faculty of Dentistry & Graduate School of Medical and Dental Sciences, Niigata University
kn-affil=

affil-num=3
en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University
kn-affil=
en-keyword=3D cancer model
kn-keyword=3D cancer model
en-keyword=preclinical study
kn-keyword=preclinical study
en-keyword=cancer treatment
kn-keyword=cancer treatment
en-keyword=quality of life
kn-keyword=quality of life
en-keyword=multidisciplinary treatment
kn-keyword=multidisciplinary treatment
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=78366
end-page=78378
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Aromug: A Mug-Type Olfactory Interface to Enhance the Sweetness Perception of Beverages
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sugary beverages are a significant contributor to sugar consumption, and their excessive consumption is associated with increased risks of elevated blood glucose levels and diabetes. Many individuals have a strong preference for sugary beverages and often find beverages with lower sugar content to be less satisfying. Attempts to switch to less sugary options are frequently short-lived, leading to a return to higher-sugar beverages. Recognizing that 75 ? 95% of taste perception is influenced by scent, we investigated a scent-based approach to reduce sugar intake while preserving the perception of sweetness. This study introduces an olfactory interface in the form of a mug named �gAromug,�h designed to emit a sweet scent in sync with the drinking action. Aromug incorporates motion sensing and scent presentation functions to enhance the perceived sweetness of a beverage, thereby encouraging a gradual reduction in sugar intake. Our experiments, involving 33 participants, demonstrated that the combined scents of sugar-free coffee and chocolate increased the perception of sweetness (p =1.641�~10?2 ). The study also found that the simultaneous presentation of scent and visual cues improved taste satisfaction and sweetness perception. Additionally, we observed variations in sweetness preference related to age and frequency of coffee consumption. It was particularly observed that people in their 20s and those who frequently drink coffee tend to perceive the taste of beverages as sweeter. This suggests a potential for Aromug to customize the scent experience based on individual preferences, offering a novel way to encourage healthier beverage choices.
en-copyright=
kn-copyright=

en-aut-name=MayumiDaiki
en-aut-sei=Mayumi
en-aut-mei=Daiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakamuraYugo
en-aut-sei=Nakamura
en-aut-mei=Yugo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsudaYuki
en-aut-sei=Matsuda
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MisakiShinya
en-aut-sei=Misaki
en-aut-mei=Shinya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YasumotoKeiichi
en-aut-sei=Yasumoto
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=

affil-num=2
en-affil=Faculty of Information Science and Electrical Engineering, Kyushu University
kn-affil=

affil-num=3
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=

affil-num=5
en-affil=Graduate School of Science and Technology, Nara Institute of Science and Technology
kn-affil=
en-keyword=Olfaction
kn-keyword=Olfaction
en-keyword=olfactory interfaces
kn-keyword=olfactory interfaces
en-keyword=olfactory display
kn-keyword=olfactory display
en-keyword=scents
kn-keyword=scents
en-keyword=taste evaluation
kn-keyword=taste evaluation
en-keyword=smell
kn-keyword=smell
en-keyword=olfactory perception
kn-keyword=olfactory perception
en-keyword=behavior change support
kn-keyword=behavior change support
END

start-ver=1.4
cd-journal=joma
no-vol=63
cd-vols=
no-issue=19
article-no=
start-page=2655
end-page=2660
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Prompt Diagnosis and Treatment of a Case of Nuclear Protein of the Testis Carcinoma Characterized by a Bronchial Lesion and High Serum Alpha-fetoprotein Level Following Genomic Testing
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Nuclear protein of the testis carcinoma (NUTC) is a rare and aggressive malignancy. We herein report a case of NUTC in the lung characterized by a bronchial lesion and elevated alpha-fetoprotein levels. A 35-year-old Japanese man presented to our institution with suspected advanced lung cancer based on a histological examination. Subsequently, next-generation sequencing (NGS) yielded a positive BRD4-NUTM1 fusion. In addition, positive NUT immunostaining of the lung biopsy specimen confirmed NUTC in the lungs. Systemic chemotherapy and radiotherapy showed a temporary response, with decreased serum alpha-fetoprotein levels. We highlight this case of a prompt diagnosis by NGS of NUTC in a young individual with a rapidly progressing tumor.
en-copyright=
kn-copyright=

en-aut-name=MatsuuraHiroaki
en-aut-sei=Matsuura
en-aut-mei=Hiroaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MakimotoGo
en-aut-sei=Makimoto
en-aut-mei=Go
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OdaNaohiro
en-aut-sei=Oda
en-aut-mei=Naohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NinomiyaKiichiro
en-aut-sei=Ninomiya
en-aut-mei=Kiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HigoHisao
en-aut-sei=Higo
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiiMasanori
en-aut-sei=Fujii
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=RaiKammei
en-aut-sei=Rai
en-aut-mei=Kammei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OhashiKadoaki
en-aut-sei=Ohashi
en-aut-mei=Kadoaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HottaKatsuyuki
en-aut-sei=Hotta
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TabataMasahiro
en-aut-sei=Tabata
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Respiratory Medicine, Fukuyama City Hospital
kn-affil=

affil-num=4
en-affil=Center for Comprehensive Genomic Medicine, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=10
en-affil=Center for Innovative Clinical Medicine, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Center for Clinical Oncology, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Hematology, Oncology, and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=NUT carcinoma
kn-keyword=NUT carcinoma
en-keyword=BRD4-NUTM1
kn-keyword=BRD4-NUTM1
en-keyword=lung cancer
kn-keyword=lung cancer
en-keyword=alpha-fetoprotein (AFP)
kn-keyword=alpha-fetoprotein (AFP)
en-keyword=immune checkpoint inhibitor
kn-keyword=immune checkpoint inhibitor
END

start-ver=1.4
cd-journal=joma
no-vol=300
cd-vols=
no-issue=3
article-no=
start-page=105679
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Methyl vinyl ketone and its analogs covalently modify PI3K and alter physiological functions by inhibiting PI3K signaling
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Reactive carbonyl species (RCS), which are abundant in the environment and are produced in vivo under stress, covalently bind to nucleophilic residues such as Cys in proteins. Disruption of protein function by RCS exposure is predicted to play a role in the development of various diseases such as cancer and metabolic disorders, but most studies on RCS have been limited to simple cytotoxicity validation, leaving their target proteins and resulting physiological changes unknown. In this study, we focused on methyl vinyl ketone (MVK), which is one of the main RCS found in cigarette smoke and exhaust gas. We found that MVK suppressed PI3K-Akt signaling, which regulates processes involved in cellular homeostasis, including cell proliferation, autophagy, and glucose metabolism. Interestingly, MVK inhibits the interaction between the epidermal growth factor receptor and PI3K. Cys656 in the SH2 domain of the PI3K p85 subunit, which is the covalently binding site of MVK, is important for this interaction. Suppression of PI3K- Akt signaling by MVK reversed epidermal growth factor- induced negative regulation of autophagy and attenuated glucose uptake. Furthermore, we analyzed the effects of the 23 RCS compounds with structures similar to MVK and showed that their analogs also suppressed PI3K-Akt signaling in a manner that correlated with their similarities to MVK. Our study demonstrates the mechanism of MVK and its analogs in suppressing PI3K-Akt signaling and modulating physiological functions, providing a model for future studies analyzing environmental reactive species.
en-copyright=
kn-copyright=

en-aut-name=MorimotoAtsushi
en-aut-sei=Morimoto
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=PanYuexuan
en-aut-sei=Pan
en-aut-mei=Yuexuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DohmaeNaoshi
en-aut-sei=Dohmae
en-aut-mei=Naoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AbikoYumi
en-aut-sei=Abiko
en-aut-mei=Yumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UchidaKoji
en-aut-sei=Uchida
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KumagaiYoshito
en-aut-sei=Kumagai
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=6
en-affil=Graduate School of Biomedical Science, Nagasaki University
kn-affil=

affil-num=7
en-affil=Laboratory of Food Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo
kn-affil=

affil-num=8
en-affil=Graduate School of Pharmaceutical Sciences, Kyushu University
kn-affil=

affil-num=9
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=phosphatidylinositol 3-kinase (PI 3-kinase)
kn-keyword=phosphatidylinositol 3-kinase (PI 3-kinase)
en-keyword=cell signaling
kn-keyword=cell signaling
en-keyword=chemical modification
kn-keyword=chemical modification
en-keyword=autophagy
kn-keyword=autophagy
en-keyword=glucose uptake
kn-keyword=glucose uptake
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=2
article-no=
start-page=563
end-page=574
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241027
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Therapeutic potential of 4-phenylbutyric acid against methylmercury-induced neuronal cell death in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Methylmercury (MeHg) is an environmental neurotoxin that induces damage to the central nervous system and is the causative agent in Minamata disease. The mechanisms underlying MeHg neurotoxicity remain largely unknown, and there is a need for effective therapeutic agents, such as those that target MeHg-induced endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), which is activated as a defense mechanism. We investigated whether intraperitoneal administration of the chemical chaperone, 4-phenylbutyric acid (4-PBA), at 120 mg/kg/day can alleviate neurotoxicity in the brains of mice administered 50 ppm MeHg in drinking water for 5 weeks. 4-PBA significantly reduced MeHg-induced ER stress, neuronal apoptosis, and neurological symptoms. Furthermore, 4-PBA was effective even when administered 2 weeks after the initiation of exposure to 30 ppm MeHg in drinking water. Our results strongly indicate that ER stress and the UPR are key processes involved in MeHg toxicity, and that 4-PBA is a novel therapeutic candidate for MeHg-induced neurotoxicity.
en-copyright=
kn-copyright=

en-aut-name=MikiRyohei
en-aut-sei=Miki
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NomuraRyosuke
en-aut-sei=Nomura
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IwawakiTakao
en-aut-sei=Iwawaki
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FujimuraMasatake
en-aut-sei=Fujimura
en-aut-mei=Masatake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Division of Cell Medicine, Department of Life Science, Medical Research Institute, Kanazawa Medical University
kn-affil=

affil-num=7
en-affil=Department of International Affairs and Research, National Institute for Minamata Disease
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Methylmercury
kn-keyword=Methylmercury
en-keyword=Neuronal cell death
kn-keyword=Neuronal cell death
en-keyword=Endoplasmic reticulum stress
kn-keyword=Endoplasmic reticulum stress
en-keyword=Unfolded protein response
kn-keyword=Unfolded protein response
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=142592
end-page=142605
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=MUSIC Spectrum Based Interference Detection, Localization, and Interference Arrival Prediction for mmWave IRS-MIMO System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=For a millimeter wave (mmWave) intelligent re-configurable surface (IRS)-MIMO system, if it can correctly detect the interference occurrence and their locations, the patterns of interference signal can be collected and learned using machine learning for the prediction of interference arrival. With the information of interference location and activity pattern, the capacity of the system can be largely improved using many techniques such as beamforming, interference cancellation, and transmission scheduling. This paper aims to detect interference occurrence using a low-complexity MUSIC (MUSIC: multiple signal classification) spectrum-based method, and then localize their sources for mmWave IRS-MIMO system. The MUSIC spectrum of wireless system can be regarded as somehow the 'signature' related to the signals transmitted from different users or interference. We utilize such property to detect the occurrence of interference, and then localize their sources in a low-complexity way. Finally, the pattern of interference occurrence can be learned to predict the interference arrival from the collected data. This paper also proposed an efficient probabilistic neural network (PNN)-based predictor for the interference arrival prediction and showed its prediction accuracy. From simulated results, our proposed method can achieve the correct results with the accuracy near to 100% when the fingerprint samples is over 10. In addition, the localization error can be within 1 m with more than 65% and 43% for Y-axis and X-axis, respectively. Finally, based on the results of the interference occurrence, the proposed PNN-based predictor for the interference arrival prediction can capture correctly the similar distribution function of the coming continuous idle status.
en-copyright=
kn-copyright=

en-aut-name=HouYafei
en-aut-sei=Hou
en-aut-mei=Yafei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YanoKazuto
en-aut-sei=Yano
en-aut-mei=Kazuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugaNorisato
en-aut-sei=Suga
en-aut-mei=Norisato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=WebberJulian
en-aut-sei=Webber
en-aut-mei=Julian
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DennoSatoshi
en-aut-sei=Denno
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakanoToshikazu
en-aut-sei=Sakano
en-aut-mei=Toshikazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

affil-num=3
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

affil-num=4
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=

affil-num=5
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=6
en-affil=Wave Engineering Laboratories, Advanced Telecommunications Research Institute International
kn-affil=
en-keyword=Interference detection
kn-keyword=Interference detection
en-keyword=MUSIC spectrum
kn-keyword=MUSIC spectrum
en-keyword=interference localization
kn-keyword=interference localization
en-keyword=prediction of interference arrival
kn-keyword=prediction of interference arrival
en-keyword=probabilistic neural network
kn-keyword=probabilistic neural network
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=413
end-page=421
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Focal Cerebral Hypoperfusion Detected by Arterial Spin-Labeled Magnetic Resonance Imaging in Patients with Migraine Presenting with Neurological Symptoms Concomitant with or without Headache
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We investigated patients with migraine or migraine variants who exhibited focal cerebral hypoperfusion on arterial spin-labeled (ASL) magnetic resonance (MR) imaging along with neurological symptoms. Fourteen patients with migraine demonstrated focal cerebral hypoperfusion. Three other patients did not have a history of recurrent headaches but exhibited comparable cerebral hypoperfusion to migraine patients on ASL-MRI in addition to neurological symptoms. Patients with migraine may present with neurological symptoms associated with cortical spreading depression during, after, or even without a headache phase. Additionally, the isolated neurological symptoms may be caused by a pathophysiology identical to that of migraine but without presenting with recurrent headaches.
en-copyright=
kn-copyright=

en-aut-name=KashiharaKenichi
en-aut-sei=Kashihara
en-aut-mei=Kenichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IrisawaMinoru
en-aut-sei=Irisawa
en-aut-mei=Minoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakaoWataru
en-aut-sei=Takao
en-aut-mei=Wataru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Okayama Neurology Clinic
kn-affil=

affil-num=2
en-affil=Department of Radiology, Okayama Kyokuto Hospital
kn-affil=

affil-num=3
en-affil=Division of Radiology, Okayama Kyokuto Hospital
kn-affil=
en-keyword=arterial spin-labeled magnetic resonance imaging
kn-keyword=arterial spin-labeled magnetic resonance imaging
en-keyword=cortical spreading depression
kn-keyword=cortical spreading depression
en-keyword=migraine complex
kn-keyword=migraine complex
en-keyword=migraine without headache
kn-keyword=migraine without headache
en-keyword=vertigo
kn-keyword=vertigo
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=5
article-no=
start-page=387
end-page=399
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202410
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Radon Inhalation on Murine Brain Proteins: Investigation Using Proteomic and Multivariate Analyses
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Radon is a known risk factor for lung cancer; however, it can be used beneficially, such as in radon therapy. We have previously reported the enhancement of antioxidant effects associated with trace amounts of oxidative stress as one of the positive biological effects of radon inhalation. However, the biological effects of radon inhalation are incompletely understood, and more detailed and comprehensive studies are required. Although several studies have used proteomics to investigate the effects of radon inhalation on body proteins, none has focused on brain proteins. In this study, we evaluated the expression status of proteins in murine brains using proteomic and multivariate analyses to identify those whose expressions changed following two days of radon inhalation at a concentration of 1,500 Bq/m3. We found associations of radon inhalation with the expressions of seven proteins related to neurotransmission and heat shock. These proteins may be proposed as biomarkers indicative of radon inhalation. Although further studies are required to obtain the detailed biological significance of these protein alterations, this study contributes to the elucidation of the biological effects of radon
inhalation as a low-dose radiation.
en-copyright=
kn-copyright=

en-aut-name=NaoeShota
en-aut-sei=Naoe
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TanakaAyumi
en-aut-sei=Tanaka
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KanzakiNorie
en-aut-sei=Kanzaki
en-aut-mei=Norie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakenakaReiju
en-aut-sei=Takenaka
en-aut-mei=Reiju
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakodaAkihiro
en-aut-sei=Sakoda
en-aut-mei=Akihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MiyajiTakaaki
en-aut-sei=Miyaji
en-aut-mei=Takaaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YamaokaKiyonori
en-aut-sei=Yamaoka
en-aut-mei=Kiyonori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KataokaTakahiro
en-aut-sei=Kataoka
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=4
en-affil=Graduate School of Health Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Ningyo-toge Environmental Engineering Center, Japan Atomic Energy Agency
kn-affil=

affil-num=6
en-affil=Advanced Science Research Center, Okayama University
kn-affil=

affil-num=7
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Faculty of Health Sciences, Okayama University
kn-affil=
en-keyword=radon inhalation
kn-keyword=radon inhalation
en-keyword=proteomics
kn-keyword=proteomics
en-keyword=multivariate analysis
kn-keyword=multivariate analysis
en-keyword=brain
kn-keyword=brain
en-keyword=oxidative stress
kn-keyword=oxidative stress
END

start-ver=1.4
cd-journal=joma
no-vol=60
cd-vols=
no-issue=5
article-no=
start-page=6736
end-page=6751
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202409
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Superior Efficiency Under PWM Harmonic Current in an Axial-Flux PM Machine for HEV/EV Traction: Comparison With a Radial-Flux PM Machine
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper evaluates the harmonic current caused by a pulse width modulation (PWM) inverter and how it affects the efficiency of a novel axial-flux permanent-magnet machine using a ferrite permanent magnet (AF-FePM) in traction applications. First, differences between the finite element analysis (FEA) and experimental results are discussed using a prototype of the proposed AF-FePM. Second, the AF-FePM is compared with a commercially available radial-flux permanent-magnet machine using a Nd-sintered magnet (RF-NdPM). For both machines, the efficiency and loss are calculated using FEA when applying the sinusoidal and harmonic currents. Additionally, we present the superior efficiency of the AF-FePM under the PWM harmonic current during a WLTC driving cycle because the designed model employs the ferrite magnet and a round copper wire, unlike the RF-NdPM. Finally, motor and inverter losses at different switching frequencies are also evaluated. This paper eventually shows that the proposed AF-FePM would be one of the suitable candidates to enhance high efficiency under PWM harmonic current condition based on comprehensive discussion.
en-copyright=
kn-copyright=

en-aut-name=TsunataRen
en-aut-sei=Tsunata
en-aut-mei=Ren
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TakemotoMasatsugu
en-aut-sei=Takemoto
en-aut-mei=Masatsugu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ImaiJun
en-aut-sei=Imai
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SaitoTatsuya
en-aut-sei=Saito
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UenoTomoyuki
en-aut-sei=Ueno
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Division of Industrial Innovation Sciences Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Industrial Innovation Sciences Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Division of Industrial Innovation Sciences Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Sumitomo Electric Industries Ltd.
kn-affil=

affil-num=5
en-affil=Sumitomo Electric Industries Ltd.
kn-affil=
en-keyword=Axial gap motor
kn-keyword=Axial gap motor
en-keyword=axial-flux machine
kn-keyword=axial-flux machine
en-keyword=carbon-fiber-reinforced plastic
kn-keyword=carbon-fiber-reinforced plastic
en-keyword=ferrite magnet
kn-keyword=ferrite magnet
en-keyword=iron loss
kn-keyword=iron loss
en-keyword=PWM drive
kn-keyword=PWM drive
en-keyword=PWM harmonic current
kn-keyword=PWM harmonic current
en-keyword=radial-flux machine
kn-keyword=radial-flux machine
en-keyword=soft magnetic composite
kn-keyword=soft magnetic composite
en-keyword=switching frequency
kn-keyword=switching frequency
en-keyword=WLTC drive
kn-keyword=WLTC drive
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=10
article-no=
start-page=1600
end-page=1609
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20241001
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Molecular Diversity of Photosensitive Protein Opsins and Their High Potential for Optogenetic Applications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Because G protein coupled receptors (GPCRs) represent the largest family of drug targets in clinical trials, GPCR signaling cascades are closely related to various physiological phenomena, attracting significant attention in pharmaceutical science. Opsins (also known as animal rhodopsins) are photoreceptive proteins containing retinal as a chromophore, which function as GPCRs and underlie the molecular basis of photoreception in animals. Recently, opsins have been progressively applied in an innovative technology called optogenetics to regulate biological activities using light. A wide variety of opsins have been identified in metazoans and characterized at the molecular and physiological levels, providing a foundation for their optogenetic applications. In this review, I briefly introduce the diversity of opsins in terms of their molecular functions, including G protein selectivity and photoreaction properties. This diversity provides a significant advantage for optically manipulating a wide variety of GPCR signaling cascades with high temporal resolution. Additionally, I discuss the rich array of opsin-based optogenetic tools used to control various physiological processes and their potential as therapeutic tools for vision restoration. Based on the introduction, I expect that the optogenetic approach will offer powerful tools to provide valuable insights into the molecular mechanisms of various physiological phenomena and next-generation treatment options for diseases beyond the capacity of traditional drugs.
en-copyright=
kn-copyright=

en-aut-name=KojimaKeiichi
en-aut-sei=Kojima
en-aut-mei=Keiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=
article-no=
start-page=1471602
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240904
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ameliorating effect of chotosan and its active component, Uncaria hook, on lipopolysaccharide-induced anxiety-like behavior in mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Introduction: In this study, we aimed to examine the effects of chotosan, a traditional Japanese botanical drug, and its active component, Uncaria hook, on anxiety-like behaviors induced by systemic inflammation in mice. <br>
Methods: To induce systemic inflammation, the mice were treated with lipopolysaccharide (LPS), a bacterial endotoxin. Prior to LPS treatment, the mice were administered chotosan or Uncaria hook orally each day for 14 days. Anxiety-like behavior of the mice was evaluated using the light-dark test 24 h after LPS treatment.<br>
Results: Repeated administration of chotosan prevented anxiety-like behavior in both normal and LPS-treated mice. Similarly, administration of Uncaria hook suppressed LPS-induced anxiety-like behavior in mice. Furthermore, treatment with tandospirone, a 5-HT1A receptor agonist, alleviated anxiety-like behavior in mice, whereas treatment with DOI, a 5-HT2A receptor agonist, enhanced anxiety-like behavior in mice. LPS treatment significantly increased serotonin (5-HT)(2A) receptor mRNA expression in the frontal cortex, whereas 5-HT1A receptor mRNA expression remained unchanged in the hippocampus. Notably, chotosan significantly suppressed the mRNA expression of 5-HT2A receptor. <br>
Discussion: These findings indicate that chotosan exerts anxiolytic-like effects in the context of inflammation-induced anxiety, potentially mediated by the inhibition of 5-HT2A receptor hyperfunction in LPS-treated mice. Consequently, we postulate that chotosan may be effective in managing inflammation-induced anxiety-like behaviors.
en-copyright=
kn-copyright=

en-aut-name=OkawaYasumasa
en-aut-sei=Okawa
en-aut-mei=Yasumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UshioSoichiro
en-aut-sei=Ushio
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IzushiYasuhisa
en-aut-sei=Izushi
en-aut-mei=Yasuhisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=4
en-affil=Department of Pharmacotherapy, School of Pharmacy, Shujitsu University
kn-affil=

affil-num=5
en-affil=Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Clinical Pharmacy, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=anxiolytic
kn-keyword=anxiolytic
en-keyword=chotosan
kn-keyword=chotosan
en-keyword=inflammation
kn-keyword=inflammation
en-keyword=serotonin receptor
kn-keyword=serotonin receptor
en-keyword=Uncaria hook
kn-keyword=Uncaria hook
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=5
article-no=
start-page=763
end-page=779
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240223
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=GRP78 Contributes to the Beneficial Effects of SGLT2 Inhibitor on Proximal Tubular Cells in DKD
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The beneficial effects of sodium?glucose cotransporter 2 (SGLT2) inhibitors on kidney function are well-known; however, their molecular mechanisms are not fully understood. We focused on 78-kDa glucose-regulated protein (GRP78) and its interaction with SGLT2 and integrin-��1 beyond the chaperone property of GRP78. In streptozotocin (STZ)-induced diabetic mouse kidneys, GRP78, SGLT2, and integrin-��1 increased in the plasma membrane fraction, while they were suppressed by canagliflozin. The altered subcellular localization of GRP78/integrin-��1 in STZ mice promoted epithelial mesenchymal transition (EMT) and fibrosis, which were mitigated by canagliflozin. High-glucose conditions reduced intracellular GRP78, increased its secretion, and caused EMT-like changes in cultured HK2 cells, which were again inhibited by canagliflozin. Urinary GRP78 increased in STZ mice, and in vitro experiments with recombinant GRP78 suggested that inflammation spread to surrounding tubular cells and that canagliflozin reversed this effect. Under normal glucose culture, canagliflozin maintained sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA) activity, promoted ER robustness, reduced ER stress response impairment, and protected proximal tubular cells. In conclusion, canagliflozin restored subcellular localization of GRP78, SGLT2, and integrin-��1 and inhibited EMT and fibrosis in DKD. In nondiabetic chronic kidney disease, canagliflozin promoted ER robustness by maintaining SERCA activity and preventing ER stress response failure, and it contributed to tubular protection.
en-copyright=
kn-copyright=

en-aut-name=NakatsukaAtsuko
en-aut-sei=Nakatsuka
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamaguchiSatoshi
en-aut-sei=Yamaguchi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=WadaJun
en-aut-sei=Wada
en-aut-mei=Jun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Division of Kidney, Diabetes and Endocrine Diseases, Okayama University Hospital
kn-affil=

affil-num=2
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=21
cd-vols=
no-issue=5
article-no=
start-page=464
end-page=473
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240827
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Terrein Exhibits Anti-tumor Activity by Suppressing Angiogenin Expression in Malignant Melanoma Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background/Aim: Malignant melanoma is a tumor with a poor prognosis that can metastasize distally at an early stage. Terrein, a metabolite produced by Aspergillus terreus, suppresses the expression of angiogenin, an angiogenic factor. However, the pharmacological effects of natural terrein have not been elucidated, because only a small amount of terrein can be extracted from large fungal cultures. In this study, we investigated the antineoplastic effects of terrein on human malignant melanoma cells and its underlying mechanisms. Materials and methods: Human malignant melanoma cell lines were cultured in the presence of terrein and analyzed. Angiogenin production was evaluated using ELISA. Ribosome biosynthesis was evaluated using silver staining of the nucleolar organizer region. Intracellular signaling pathways were analyzed using western blotting. Malignant melanoma cells were transplanted subcutaneously into the backs of nude mice. The tumors were removed at 5 weeks and analyzed histopathologically. Results: Terrein inhibited angiogenin expression, proliferation, migration, invasion, and ribosome biosynthesis in malignant melanoma cells. Terrein was shown to inhibit tumor growth and angiogenesis in animal models. Conclusion: This study demonstrated that terrein has anti-tumor effects against malignant melanoma. Furthermore, chemically synthesized non-natural terrein can be mass-produced and serve as a novel potential anti-tumor drug candidate.
en-copyright=
kn-copyright=

en-aut-name=HIROSETAIRA
en-aut-sei=HIROSE
en-aut-mei=TAIRA
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KUNISADAYUKI
en-aut-sei=KUNISADA
en-aut-mei=YUKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KADOYAKOICHI
en-aut-sei=KADOYA
en-aut-mei=KOICHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MANDAIHIROKI
en-aut-sei=MANDAI
en-aut-mei=HIROKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SAKAMOTOYUMI
en-aut-sei=SAKAMOTO
en-aut-mei=YUMI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OBATAKYOICHI
en-aut-sei=OBATA
en-aut-mei=KYOICHI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ONOKISHO
en-aut-sei=ONO
en-aut-mei=KISHO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TAKAKURAHIROAKI
en-aut-sei=TAKAKURA
en-aut-mei=HIROAKI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OMORIKAZUHIRO
en-aut-sei=OMORI
en-aut-mei=KAZUHIRO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TAKASHIBASHOGO
en-aut-sei=TAKASHIBA
en-aut-mei=SHOGO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=SUGASEIJI
en-aut-sei=SUGA
en-aut-mei=SEIJI
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=IBARAGISOICHIRO
en-aut-sei=IBARAGI
en-aut-mei=SOICHIRO
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Pharmacy, Faculty of Pharmacy, Gifu University of Medical Science
kn-affil=

affil-num=5
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Pathophysiology-Periodontal Science, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Oral and Maxillofacial Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Head and neck cancer
kn-keyword=Head and neck cancer
en-keyword=oral cancer
kn-keyword=oral cancer
en-keyword=malignant melanoma
kn-keyword=malignant melanoma
en-keyword=angiogenin
kn-keyword=angiogenin
en-keyword=terrein
kn-keyword=terrein
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=20521
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240903
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Suppression of PTBP1 in hippocampal astrocytes promotes neurogenesis and ameliorates recognition memory in mice with cerebral ischemia
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The therapeutic potential of suppressing polypyrimidine tract-binding protein 1 (Ptbp1) messenger RNA by viral transduction in a post-stroke dementia mouse model has not yet been examined. In this study, 3 days after cerebral ischemia, we injected a viral vector cocktail containing adeno-associated virus (AAV)-pGFAP-mCherry and AAV-pGFAP-CasRx (control vector) or a cocktail of AAV-pGFAP-mCherry and AAV-pGFAP-CasRx-SgRNA-(Ptbp1) (1:5, 1.0 x 1011 viral genomes) into post-stroke mice via the tail vein. We observed new mCherry/NeuN double-positive neuron-like cells in the hippocampus 56 days after cerebral ischemia. A portion of mCherry/GFAP double-positive astrocyte-like glia could have been converted into new mCherry/NeuN double-positive neuron-like cells with morphological changes. The new neuronal cells integrated into the dentate gyrus and recognition memory was significantly ameliorated. These results demonstrated that the in vivo conversion of hippocampal astrocyte-like glia into functional new neurons by the suppression of Ptbp1 might be a therapeutic strategy for post-stroke dementia.
en-copyright=
kn-copyright=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=CasRx
kn-keyword=CasRx
en-keyword=Hippocampal neurogenesis
kn-keyword=Hippocampal neurogenesis
en-keyword=In vivo direct reprogramming
kn-keyword=In vivo direct reprogramming
en-keyword=Ischemic stroke
kn-keyword=Ischemic stroke
en-keyword=PHP.eB
kn-keyword=PHP.eB
en-keyword=Ptbp1
kn-keyword=Ptbp1
en-keyword=Recognition memory
kn-keyword=Recognition memory
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=16
article-no=
start-page=9038
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240820
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Quercetin Attenuates Acetaldehyde-Induced Cytotoxicity via the Heme Oxygenase-1-Dependent Antioxidant Mechanism in Hepatocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=It is still unclear whether or how quercetin influences the toxic events induced by acetaldehyde in hepatocytes, though quercetin has been reported to mitigate alcohol-induced mouse liver injury. In this study, we evaluated the modulating effect of quercetin on the cytotoxicity induced by acetaldehyde in mouse hepatoma Hepa1c1c7 cells, the frequently used cellular hepatocyte model. The pretreatment with quercetin significantly inhibited the cytotoxicity induced by acetaldehyde. The treatment with quercetin itself had an ability to enhance the total ALDH activity, as well as the ALDH1A1 and ALDH3A1 gene expressions. The acetaldehyde treatment significantly enhanced the intracellular reactive oxygen species (ROS) level, whereas the quercetin pretreatment dose-dependently inhibited it. Accordingly, the treatment with quercetin itself significantly up-regulated the representative intracellular antioxidant-related gene expressions, including heme oxygenase-1 (HO-1), glutamate-cysteine ligase, catalytic subunit (GCLC), and cystine/glutamate exchanger (xCT), that coincided with the enhancement of the total intracellular glutathione (GSH) level. Tin protoporphyrin IX (SNPP), a typical HO-1 inhibitor, restored the quercetin-induced reduction in the intracellular ROS level, whereas buthionine sulphoximine, a representative GSH biosynthesis inhibitor, did not. SNPP also cancelled the quercetin-induced cytoprotection against acetaldehyde. These results suggest that the low-molecular-weight antioxidants produced by the HO-1 enzymatic reaction are mainly attributable to quercetin-induced cytoprotection.
en-copyright=
kn-copyright=

en-aut-name=LiKexin
en-aut-sei=Li
en-aut-mei=Kexin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KidawaraMinori
en-aut-sei=Kidawara
en-aut-mei=Minori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ChenQiguang
en-aut-sei=Chen
en-aut-mei=Qiguang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MunemasaShintaro
en-aut-sei=Munemasa
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MurataYoshiyuki
en-aut-sei=Murata
en-aut-mei=Yoshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraToshiyuki
en-aut-sei=Nakamura
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=7
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=
en-keyword=quercetin
kn-keyword=quercetin
en-keyword=acetaldehyde
kn-keyword=acetaldehyde
en-keyword=glutathione
kn-keyword=glutathione
en-keyword=aldehyde dehydrogenase
kn-keyword=aldehyde dehydrogenase
en-keyword=heme oxygenase-1
kn-keyword=heme oxygenase-1
END

start-ver=1.4
cd-journal=joma
no-vol=476
cd-vols=
no-issue=11
article-no=
start-page=1761
end-page=1775
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240829
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The role of GABA in modulation of taste signaling within the taste bud
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Taste buds contain 2 types of GABA-producing cells: sour-responsive Type III cells and glial-like Type I cells. The physiological role of GABA, released by Type III cells is not fully understood. Here, we investigated the role of GABA released from Type III cells using transgenic mice lacking the expression of GAD67 in taste bud cells (Gad67-cKO mice). Immunohistochemical experiments confirmed the absence of GAD67 in Type III cells of Gad67-cKO mice. Furthermore, no difference was observed in the expression and localization of cell type markers, ectonucleoside triphosphate diphosphohydrolase 2 (ENTPD2), gustducin, and carbonic anhydrase 4 (CA4) in taste buds between wild-type (WT) and Gad67-cKO mice. Short-term lick tests demonstrated that both WT and Gad67-cKO mice exhibited normal licking behaviors to each of the five basic tastants. Gustatory nerve recordings from the chorda tympani nerve demonstrated that both WT and Gad67-cKO mice similarly responded to five basic tastants when they were applied individually. However, gustatory nerve responses to sweet?sour mixtures were significantly smaller than the sum of responses to each tastant in WT mice but not in Gad67-cKO mice. In summary, elimination of GABA signalling by sour-responsive Type III taste cells eliminates the inhibitory cell?cell interactions seen with application of sour?sweet mixtures.
en-copyright=
kn-copyright=

en-aut-name=MikamiAyaka
en-aut-sei=Mikami
en-aut-mei=Ayaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HuangHai
en-aut-sei=Huang
en-aut-mei=Hai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HyodoAiko
en-aut-sei=Hyodo
en-aut-mei=Aiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HorieKengo
en-aut-sei=Horie
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YasumatsuKeiko
en-aut-sei=Yasumatsu
en-aut-mei=Keiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MitohYoshihiro
en-aut-sei=Mitoh
en-aut-mei=Yoshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IidaSeiji
en-aut-sei=Iida
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Tokyo Dental Junior College
kn-affil=

affil-num=6
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Oral and Maxillofacial Reconstructive Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Gamma-aminobutyric acid
kn-keyword=Gamma-aminobutyric acid
en-keyword=Taste buds
kn-keyword=Taste buds
en-keyword=Glutamate decarboxylase
kn-keyword=Glutamate decarboxylase
en-keyword=Taste mixture
kn-keyword=Taste mixture
en-keyword=Sour
kn-keyword=Sour
en-keyword=Sweet
kn-keyword=Sweet
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=14543
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240624
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Cervical spinal cord stimulation exerts anti-epileptic effects in a rat model of epileptic seizure through the suppression of CCL2-mediated cascades
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epidural spinal cord stimulation (SCS) is indicated for the treatment of intractable pain and is widely used in clinical practice. In previous basic research, the therapeutic effects of SCS have been demonstrated for epileptic seizure. However, the mechanism has not yet been elucidated. In this study, we investigated the therapeutic effect of SCS and the influence of epileptic seizure. First, SCS in the cervical spine was performed. The rats were divided into four groups: control group and treatment groups with SCS conducted at 2, 50, and 300 Hz frequency. Two days later, convulsions were induced by the intraperitoneal administration of kainic acid, followed by video monitoring to assess seizures. We also evaluated glial cells in the hippocampus by fluorescent immunostaining, electroencephalogram measurements, and inflammatory cytokines such as C-C motif chemokine ligand 2 (CCL2) by quantitative real-time polymerase chain reaction. Seizure frequency and the number of glial cells were significantly lower in the 300 Hz group than in the control group. SCS at 300 Hz decreased gene expression level of CCL2, which induces monocyte migration. SCS has anti-seizure effects by inhibiting CCL2-mediated cascades. The suppression of CCL2 and glial cells may be associated with the suppression of epileptic seizure.
en-copyright=
kn-copyright=

en-aut-name=OkazakiYosuke
en-aut-sei=Okazaki
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SasakiTatsuya
en-aut-sei=Sasaki
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HosomotoKakeru
en-aut-sei=Hosomoto
en-aut-mei=Kakeru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TanimotoShun
en-aut-sei=Tanimoto
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KawaiKoji
en-aut-sei=Kawai
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NagaseTakayuki
en-aut-sei=Nagase
en-aut-mei=Takayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YabunoSatoru
en-aut-sei=Yabuno
en-aut-mei=Satoru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KinKyohei
en-aut-sei=Kin
en-aut-mei=Kyohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SasadaSusumu
en-aut-sei=Sasada
en-aut-mei=Susumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TanakaShota
en-aut-sei=Tanaka
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurosurgery, Kure Kyosai Hospital
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of Neurosurgery, Okayama Rosai Hospital
kn-affil=
en-keyword=Epileptic seizure
kn-keyword=Epileptic seizure
en-keyword=Glial cells
kn-keyword=Glial cells
en-keyword=Spinal cord stimulation
kn-keyword=Spinal cord stimulation
en-keyword=C-C motif chemokine ligand 2
kn-keyword=C-C motif chemokine ligand 2
END

start-ver=1.4
cd-journal=joma
no-vol=38
cd-vols=
no-issue=2
article-no=
start-page=394
end-page=408
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200221
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The neurotoxicity of psychoactive phenethylamines �g2C series�h in cultured monoaminergic neuronal cell lines
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose The aim of this study was to evaluate the neurotoxicity of psychoactive abused 2,5-dimethoxy-substituted phenethylamines �g2C series�h in monoaminergic neurons.<br>
Methods After the exposure to �g2C series�h, 2,5-dimethoxy-4-propylthiophenethylamine (2C-T-7), 2,5-dimethoxy-4-isopropylthiophenethylamine (2C-T-4), 2,5-dimethoxy-4-ethylthiophenthylamine (2C-T-2), 2,5-dimethoxy-4-iodophenethylamine (2C-I) or 2,5-dimethoxy-4-chlorophenethylamine (2C-C), we examined their neurotoxicity, morphological changes, and effects of concomitant exposure to 3,4-methylenedioxymethamphetamine (MDMA) or methamphetamine (METH), using cultured neuronal dopaminergic CATH.a cells and serotonin-containing B65 cells.<br>
Results Single dose exposure to �g2C series�h for 24 h showed significant cytotoxicity as increase in lactate dehydrogenase (LDH) release from both monoaminergic neurons: 2C-T-7, 2C-C (EC50; 100 ?M)?>?2C-T-2 (150 ?M), 2C-T-4 (200 ?M)?>?2C-I (250 ?M) in CATH.a cells and 2C-T-7, 2C-I (150 ?M)?>?2C-T-2 (250 ?M)?>?2C-C, 2C-T-4 (300 ?M) in B65 cells. The �g2C series�h-induced neurotoxicity in both cells was higher than that of MDMA or METH (EC50:???1?2 mM). In addition, apoptotic morphological changes were observed at relatively lower concentrations of �g2C series�h. The concomitant exposure to non-toxic dose of MDMA or METH synergistically enhanced 2C series drugs-induced LDH release and apoptotic changes in B65 cells, but to a lesser extent in CATH.a cells. In addition, the lower dose of 2C-T-7, 2C-T-2 or 2C-I promoted reactive oxygen species production in the mitochondria of B65 cells, even at the early stages (3 h) without apparent morphological changes.<br>
Conclusion The 2,5-dimethoxy-substitution of �g2C series�h induced severe neurotoxicity in both dopaminergic and serotonin-containing neurons. The non-toxic dose of MDMA or METH synergistically enhanced its neurotoxicity in serotonergic neurons.
en-copyright=
kn-copyright=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FunadaMasahiko
en-aut-sei=Funada
en-aut-mei=Masahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Division of Drug Dependence, National Institute of Mental Health, National Center of Neurology and Psychiatry
kn-affil=
en-keyword=Psychoactive drugs
kn-keyword=Psychoactive drugs
en-keyword=2,5-Dimethoxy-substituted phenethylamines
kn-keyword=2,5-Dimethoxy-substituted phenethylamines
en-keyword=Neurotoxicity
kn-keyword=Neurotoxicity
en-keyword=Serotonin-containing  neurons
kn-keyword=Serotonin-containing  neurons
en-keyword=Dopamine neurons
kn-keyword=Dopamine neurons
en-keyword=Reactive oxygen species
kn-keyword=Reactive oxygen species
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=121
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pure argyrophilic grain disease revisited: independent effects on limbic, neocortical, and striato-pallido-nigral degeneration and the development of dementia in a series with a low to moderate Braak stage
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Agyrophilic grains (AGs) are age-related limbic-predominant lesions in which four-repeat tau is selectively accumulated. Because previous methodologically heterogeneous studies have demonstrated inconsistent findings on the relationship between AGs and dementia, whether AGs affect cognitive function remains unclear. To address this question, we first comprehensively evaluated the distribution and quantity of Gallyas-positive AGs and the severity of neuronal loss in the limbic, neocortical, and subcortical regions in 30 cases of pure argyrophilic grain disease (pAGD) in Braak stages I-IV and without other degenerative diseases, and 34 control cases that had only neurofibrillary tangles with Braak stages I-IV and no or minimal A beta deposits. Then, we examined whether AGs have independent effects on neuronal loss and dementia by employing multivariate ordered logistic regression and binomial logistic regression. Of 30 pAGD cases, three were classified in diffuse form pAGD, which had evident neuronal loss not only in the limbic region but also in the neocortex and subcortical nuclei. In all 30 pAGD cases, neuronal loss developed first in the amygdala, followed by temporo-frontal cortex, hippocampal CA1, substantia nigra, and finally, the striatum and globus pallidus with the progression of Saito AG stage. In multivariate analyses of 30 pAGD and 34 control cases, the Saito AG stage affected neuronal loss in the amygdala, hippocampal CA1, temporo-frontal cortex, striatum, globus pallidus, and substantia nigra independent of the age, Braak stage, and limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) stage. In multivariate analyses of 23 pAGD and 28 control cases that lacked two or more lacunae and/or one or more large infarctions, 100 or more AGs per x 400 visual field in the amygdala (OR 10.02, 95% CI 1.12-89.43) and hippocampal CA1 (OR 12.22, 95% CI 1.70-87.81), and the presence of AGs in the inferior temporal cortex (OR 8.18, 95% CI 1.03-65.13) affected dementia independent of age, moderate Braak stages (III-IV), and LATE-NC. Given these findings, the high density of limbic AGs and the increase of AGs in the inferior temporal gyrus may contribute to the occurrence of dementia through neuronal loss, at least in cases in a low to moderate Braak stage.
en-copyright=
kn-copyright=

en-aut-name=YokotaOsamu
en-aut-sei=Yokota
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiTomoko
en-aut-sei=Miki
en-aut-mei=Tomoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=Nakashima-YasudaHanae
en-aut-sei=Nakashima-Yasuda
en-aut-mei=Hanae
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IshizuHideki
en-aut-sei=Ishizu
en-aut-mei=Hideki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HaraguchiTakashi
en-aut-sei=Haraguchi
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaChikako
en-aut-sei=Ikeda
en-aut-mei=Chikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HasegawaMasato
en-aut-sei=Hasegawa
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MiyashitaAkinori
en-aut-sei=Miyashita
en-aut-mei=Akinori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IkeuchiTakeshi
en-aut-sei=Ikeuchi
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NishikawaNaoto
en-aut-sei=Nishikawa
en-aut-mei=Naoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=TakenoshitaShintaro
en-aut-sei=Takenoshita
en-aut-mei=Shintaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SudoKoichiro
en-aut-sei=Sudo
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TeradaSeishi
en-aut-sei=Terada
en-aut-mei=Seishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=TakakiManabu
en-aut-sei=Takaki
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

affil-num=1
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Okayama University Medical School 
kn-affil=

affil-num=4
en-affil=Okayama University Medical School 
kn-affil=

affil-num=5
en-affil=Department of Neurology, National Hospital Organization Minami Okayama Medical Center
kn-affil=

affil-num=6
en-affil=Okayama University Medical School 
kn-affil=

affil-num=7
en-affil=Dementia Research Project, Tokyo Metropolitan Institute of Medical Science
kn-affil=

affil-num=8
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=9
en-affil=Department of Molecular Genetics, Brain Research Institute, Niigata University
kn-affil=

affil-num=10
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=11
en-affil=Department of Neuropsychiatry, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of Psychiatry, Tosa Hospital
kn-affil=

affil-num=13
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Argyrophilic grain
kn-keyword=Argyrophilic grain
en-keyword=Globus pallidus
kn-keyword=Globus pallidus
en-keyword=Hippocampal sclerosis
kn-keyword=Hippocampal sclerosis
en-keyword=Striatum
kn-keyword=Striatum
en-keyword=Substantia nigra
kn-keyword=Substantia nigra
en-keyword=Subthalamic nucleus
kn-keyword=Subthalamic nucleus
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=1
article-no=
start-page=341
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240813
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Pathological findings in enucleated eyes of patients with neurofibromatosis type 1: report of a case with 15-year follow-up and review of 14 patients in the literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Backgrounds Iris nodules are frequently noted as clinical manifestations of neurofibromatosis type 1 but the other intraocular manifestations are rare. The purpose of this study is to present a patient with a phthisic eye who underwent enucleation for a cosmetic reason after 15-year follow-up and also to review 14 patients with enucleation described in the literature.<br>
Case presentation A 17-year-old man with neurofibromatosis type 1 from infancy underwent the enucleation of phthisic left eye and also had the resection of eyelid subcutaneous mass lesions on the left side for a cosmetic reason. He had undergone four-time preceding surgeries for eyelid and orbital mass reduction on the left side in childhood and had developed total retinal detachment 10 years previously. Pathologically, the enucleated eye showed massive retinal gliosis positive for both S-100 and glial fibrillary acidic protein (GFAP) in the area with involvement of the detached retinal neuronal layer, together with a more fibrotic lesion along the choroid which were, in contrast, negative for both S-100 and GFAP. The choroid, ciliary body, and iris did not show apparent neurofibroma while episcleral neurofibroma was present.<br>
Literature review In review of enucleated eyes of 14 patients in the literature, buphthalmic eyes with early-onset glaucoma on the unilateral side was clinically diagnosed in 9 patients who frequently showed varying extent of hemifacial neurofibromatosis which involved the eyelid and orbit on the same side. Pathologically, neurofibromas in varying extent were found in the choroid of 12 patients. One patient showed choroidal malignant melanoma on the left side and fusiform enlargement of the optic nerve on the right side suspected of optic nerve glioma. The phthisic eye in another patient showed massive retinal gliosis similar to the present patient.<br>
Conclusions In summary of the 15 patients with neurofibromatosis type 1, including the present patient, buphthalmic or phthisic eyes with no vision were enucleated for cosmetic reasons and showed choroidal neurofibroma in most patients and massive retinal gliosis in two patients including the present patient.
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NishidaKenji
en-aut-sei=Nishida
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TanakaTakehiro
en-aut-sei=Tanaka
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SenoTakaya
en-aut-sei=Seno
en-aut-mei=Takaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamadaKiyoshi
en-aut-sei=Yamada
en-aut-mei=Kiyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OnoShigeki
en-aut-sei=Ono
en-aut-mei=Shigeki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Pathology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, General Medical Center, Kawasaki Medical School
kn-affil=
en-keyword=Neurofibromatosis type 1
kn-keyword=Neurofibromatosis type 1
en-keyword=Enucleation
kn-keyword=Enucleation
en-keyword=Eye
kn-keyword=Eye
en-keyword=Pathology
kn-keyword=Pathology
en-keyword=Massive retinal gliosis
kn-keyword=Massive retinal gliosis
en-keyword=Choroidal neurofibroma
kn-keyword=Choroidal neurofibroma
en-keyword=Phthisis
kn-keyword=Phthisis
en-keyword=Buphthalmos
kn-keyword=Buphthalmos
en-keyword=Malignant melanoma
kn-keyword=Malignant melanoma
en-keyword=Cosmetic surgery
kn-keyword=Cosmetic surgery
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=14
article-no=
start-page=4099
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240713
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Importance of Blood Glucose Measurement for Predicting the Prognosis of Long COVID: A Retrospective Study in Japan
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: The present study aimed to clarify the effects of a hyperglycemic condition on the clinical consequences of long COVID. Methods: Among 643 patients who visited the outpatient clinic of our hospital from February 2021 to September 2023, long COVID patients were classified into a hyperglycemic (HG) group with casual blood glucose levels above 140 mg/dL and a normoglycemic (NG) group. The patients' backgrounds, clinical symptoms, health status including the QOL evaluation scale (EQ-5D-5L), self-rating depression scale (SDS), and F-scale questionnaire (FSSG), blood test data, and recovery periods were analyzed. Results: The NG group included 607 patients with long COVID and the HG group included 36 patients with long COVID. Patients in the HG group were older than those in the NG group (55 vs. 41 years; p < 0.001) and included a larger percentage of males (67% vs. 44%; p = 0.009). The HG group had a larger percentage of patients with moderate-to-severe conditions in the acute infection phase (28% vs. 12%; p = 0.008), a higher BMI (25 vs. 22 kg/m(2); p < 0.001), higher blood pressure (138/81 vs. 122/72 mmHg; p < 0.001), and a larger percentage of patients with an alcohol drinking habit (53% vs. 34%; p = 0.031). Long COVID symptoms and self-rated scales were not differed between the two groups; however, the laboratory data showed that liver and renal functions and metabolic data were significantly worse in the HG group. Although there was no apparent difference between the two groups in duration from the infection to the first visit, the HG group had a significantly longer period of recovery from long COVID (median period of 421 vs. 294 days; p = 0.019). Conclusion: A hyperglycemic state associated with other lifestyle-related diseases is associated with the prolongation of recovery from long COVID.
en-copyright=
kn-copyright=

en-aut-name=YokoyamaSho
en-aut-sei=Yokoyama
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=KishidaMasayuki
en-aut-sei=Kishida
en-aut-mei=Masayuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=14
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=15
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=blood glucose
kn-keyword=blood glucose
en-keyword=diabetes mellitus
kn-keyword=diabetes mellitus
en-keyword=long COVID
kn-keyword=long COVID
en-keyword=omicron variant
kn-keyword=omicron variant
en-keyword=post-COVID-19 condition
kn-keyword=post-COVID-19 condition
END

start-ver=1.4
cd-journal=joma
no-vol=47
cd-vols=
no-issue=6
article-no=
start-page=1119
end-page=1122
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240605
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Epigenetic Regulation of Carbonic Anhydrase 9 Expression by Nitric Oxide in Human Small Airway Epithelial Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=DNA methylation is a crucial epigenetic modification that regulates gene expression and determines cell fate; however, the triggers that alter DNA methylation levels remain unclear. Recently, we showed that S-nitrosylation of DNA methyltransferase (DNMT) induces DNA hypomethylation and alters gene expression. Furthermore, we identified DBIC, a specific inhibitor of S-nitrosylation of DNMT3B, to suppress nitric oxide (NO)-induced gene alterations. However, it remains unclear how NO-induced DNA hypomethylation regulates gene expression and whether this mechanism is maintained in normal cells and triggers disease-related changes. To address these issues, we focused on carbonic anhydrase 9 (CA9), which is upregulated under nitrosative stress in cancer cells. We pharmacologically evaluated its regulatory mechanisms using human small airway epithelial cells (SAECs) and DBIC. We demonstrated that nitrosative stress promotes the recruitment of hypoxia-inducible factor 1 alpha to the CA9 promoter region and epigenetically induces CA9 expression in SAECs. Our results suggest that nitrosative stress is a key epigenetic regulator that may cause diseases by altering normal cell function.
en-copyright=
kn-copyright=

en-aut-name=MoriyaYuto
en-aut-sei=Moriya
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=nitric oxide
kn-keyword=nitric oxide
en-keyword=human small airway epithelial cell
kn-keyword=human small airway epithelial cell
en-keyword=epigenetics
kn-keyword=epigenetics
en-keyword=DNA methylation
kn-keyword=DNA methylation
en-keyword=carbonic anhydrase 9
kn-keyword=carbonic anhydrase 9
en-keyword=hypoxia-inducible factor 1 alpha
kn-keyword=hypoxia-inducible factor 1 alpha
END

start-ver=1.4
cd-journal=joma
no-vol=39
cd-vols=
no-issue=5
article-no=
start-page=463
end-page=483
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240731
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Detailed Re-Examination of the Period Gene Rescue Experiments Shows That Four to Six Cryptochrome-Positive Posterior Dorsal Clock Neurons (DN1p) of Drosophila melanogaster Can Control Morning and Evening Activity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Animal circadian clocks play a crucial role in regulating behavioral adaptations to daily environmental changes. The fruit fly Drosophila melanogaster exhibits 2 prominent peaks of activity in the morning and evening, known as morning (M) and evening (E) peaks. These peaks are controlled by 2 distinct circadian oscillators located in separate groups of clock neurons in the brain. To investigate the clock neurons responsible for the M and E peaks, a cell-specific gene expression system, the GAL4-UAS system, has been commonly employed. In this study, we re-examined the two-oscillator model for the M and E peaks of Drosophila by utilizing more than 50 Gal4 lines in conjunction with the UAS-period16 line, which enables the restoration of the clock function in specific cells in the period (per) null mutant background. Previous studies have indicated that the group of small ventrolateral neurons (s-LNv) is responsible for controlling the M peak, while the other group, consisting of the 5th ventrolateral neuron (5th LNv) and the three cryptochrome (CRY)-positive dorsolateral neurons (LNd), is responsible for the E peak. Furthermore, the group of posterior dorsal neurons 1 (DN1p) is thought to also contain M and E oscillators. In this study, we found that Gal4 lines directed at the same clock neuron groups can lead to different results, underscoring the fact that activity patterns are influenced by many factors. Nevertheless, we were able to confirm previous findings that the entire network of circadian clock neurons controls M and E peaks, with the lateral neurons playing a dominant role. In addition, we demonstrate that 4 to 6 CRY-positive DN1p cells are sufficient to generate M and E peaks in light-dark cycles and complex free-running rhythms in constant darkness. Ultimately, our detailed screening could serve as a catalog to choose the best Gal4 lines that can be used to rescue per in specific clock neurons.
en-copyright=
kn-copyright=

en-aut-name=SekiguchiManabu
en-aut-sei=Sekiguchi
en-aut-mei=Manabu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ReinhardNils
en-aut-sei=Reinhard
en-aut-mei=Nils
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FukudaAyumi
en-aut-sei=Fukuda
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KatohShun
en-aut-sei=Katoh
en-aut-mei=Shun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RiegerDirk
en-aut-sei=Rieger
en-aut-mei=Dirk
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=Helfrich-F?rsterCharlotte
en-aut-sei=Helfrich-F?rster
en-aut-mei=Charlotte
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=6
en-affil=Neurobiology and Genetics, Theodor-Boveri Institute, Biocenter, University of W?rzburg
kn-affil=

affil-num=7
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=period
kn-keyword=period
en-keyword=GAL4-UAS
kn-keyword=GAL4-UAS
en-keyword=clock neuron
kn-keyword=clock neuron
en-keyword=activity rhythm
kn-keyword=activity rhythm
en-keyword=two-oscillator model
kn-keyword=two-oscillator model
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=13
article-no=
start-page=3809
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240628
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Changes in Working Situations of Employed Long COVID Patients: Retrospective Study in Japanese Outpatient Clinic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: The present study aimed to uncover the impact of long COVID on the working situations of Japanese patients. Methods: Changes in the working situations of the patients who visited our long COVID clinic were evaluated from medical records for the aspects of physical status, quality of life (QOL), and mental conditions. <br>
Results: Of 846 long COVID patients who visited our clinic from February 2021 to December 2023, 545 employed patients aged between 18 and 65 years were included in this study. A total of 295 patients (54.1%) with long COVID (median age: 43 years, female: 55.6%) experienced changes in their working status. Those patients included 220 patients (40.4%) who took a leave of absence, 53 patients (9.7%) who retired, and 22 patients (4%) with reduced working hours. Most of the patients (93.2%) with changes in working conditions had mild disease severity in the acute phase of COVID-19. The majority of those patients with mild disease severity (58.8%) were infected in the Omicron-variant phase and included 65.3% of the female patients. The major symptoms in long COVID patients who had changes in their working situations were fatigue, insomnia, headache, and dyspnea. Scores indicating fatigue and QOL were worsened in long COVID patients who had changes in their working situations. In addition, 63.7% of the long COVID patients with changes in their working situations had decreases in their incomes. <br>
Conclusions: Changes in the working situation of long COVID patients who were employed had a negative impact on the maintenance of their QOL.
en-copyright=
kn-copyright=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakaseRyosuke
en-aut-sei=Takase
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=OmuraDaisuke
en-aut-sei=Omura
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=employment
kn-keyword=employment
en-keyword=job retirement
kn-keyword=job retirement
en-keyword=leave of absence
kn-keyword=leave of absence
en-keyword=long COVID
kn-keyword=long COVID
en-keyword=omicron variant
kn-keyword=omicron variant
en-keyword=post-COVID-19 condition
kn-keyword=post-COVID-19 condition
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=13
article-no=
start-page=7398
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240705
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The oral detection of sugars relies on two types of receptor systems. The first is the G-protein-coupled receptor TAS1R2/TAS1R3. When activated, this receptor triggers a downstream signaling cascade involving gustducin, phospholipase C beta 2 (PLC beta 2), and transient receptor potential channel M5 (TRPM5). The second type of receptor is the glucose transporter. When glucose enters the cell via this transporter, it is metabolized to produce ATP. This ATP inhibits the opening of KATP channels, leading to cell depolarization. Beside these receptor systems, sweet-sensitive taste cells have mechanisms to regulate their sensitivity to sweet substances based on internal and external states of the body. Sweet taste receptors are not limited to the oral cavity; they are also present in extraoral organs such as the gastrointestinal tract, pancreas, and brain. These extraoral sweet receptors are involved in various functions, including glucose absorption, insulin release, sugar preference, and food intake, contributing to the maintenance of energy homeostasis. Additionally, sweet receptors may have unique roles in certain organs like the trachea and bone. This review summarizes past and recent studies on sweet receptor systems, exploring the molecular mechanisms and physiological functions of sweet (sugar) detection in both oral and extraoral organs.
en-copyright=
kn-copyright=

en-aut-name=YoshidaRyusuke
en-aut-sei=Yoshida
en-aut-mei=Ryusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NinomiyaYuzo
en-aut-sei=Ninomiya
en-aut-mei=Yuzo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=energy homeostasis
kn-keyword=energy homeostasis
en-keyword=T1R3
kn-keyword=T1R3
en-keyword=GLUT
kn-keyword=GLUT
en-keyword=SGLT
kn-keyword=SGLT
en-keyword=sugar
kn-keyword=sugar
END

start-ver=1.4
cd-journal=joma
no-vol=137
cd-vols=
no-issue=11
article-no=
start-page=jcs261977
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240612
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Toxicity of the model protein 3�~GFP arises from degradation overload, not from aggregate formation
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although protein aggregation can cause cytotoxicity, such aggregates can also form to mitigate cytotoxicity from misfolded proteins, although the nature of these contrasting aggregates remains unclear. We previously found that overproduction (op) of a three green fluorescent protein-linked protein (3�~GFP) induces giant aggregates and is detrimental to growth. Here, we investigated the mechanism of growth inhibition by 3�~GFP-op using non-aggregative 3�~MOX-op as a control in Saccharomyces cerevisiae. The 3�~GFP aggregates were induced by misfolding, and 3�~GFP-op had higher cytotoxicity than 3�~MOX-op because it perturbed the ubiquitin-proteasome system. Static aggregates formed by 3�~GFP-op dynamically trapped Hsp70 family proteins (Ssa1 and Ssa2 in yeast), causing the heat-shock response. Systematic analysis of mutants deficient in the protein quality control suggested that 3�~GFP-op did not cause a critical Hsp70 depletion and aggregation functioned in the direction of mitigating toxicity. Artificial trapping of essential cell cycle regulators into 3�~GFP aggregates caused abnormalities in the cell cycle. In conclusion, the formation of the giant 3�~GFP aggregates itself is not cytotoxic, as it does not entrap and deplete essential proteins. Rather, it is productive, inducing the heat-shock response while preventing an overload to the degradation system.
en-copyright=
kn-copyright=

en-aut-name=NambaShotaro
en-aut-sei=Namba
en-aut-mei=Shotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaHisao
en-aut-sei=Moriya
en-aut-mei=Hisao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Graduate School of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Aggregation
kn-keyword=Aggregation
en-keyword=Fluorescent protein
kn-keyword=Fluorescent protein
en-keyword=Hsp70
kn-keyword=Hsp70
en-keyword=Overproduction
kn-keyword=Overproduction
en-keyword=Toxicity
kn-keyword=Toxicity
en-keyword=Yeast
kn-keyword=Yeast
END

start-ver=1.4
cd-journal=joma
no-vol=820
cd-vols=
no-issue=
article-no=
start-page=137598
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240118
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Neurogenesis impairment with glial activation in the hippocampus-connected regions of intracerebroventricular streptozotocin-injected mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Adult neurogenesis in the hippocampus and subventricular zone (SVZ) is impaired by intracerebroventricular administration of streptozotocin (icv-STZ) to rodents. Although neural cells in the several brain regions which connect with the hippocampus or SVZ is thought to be involved in the adult neurogenesis, few studies have investigated morphological alterations of glial cells in these areas. The present study revealed that icv-STZ induces reduction of neural progenitor cells and a dramatic increase in reactive astrocytes and microglia especially in the hippocampus and various hippocampus-connected brain areas. In contrast, there was no significant neuronal damage excluding demyelination of the stria medullaris. The results indicate the hippocampal neurogenesis impairment of this model might be occurred by activated glial cells in the hippocampus, or hippocampus-connected regions.
en-copyright=
kn-copyright=

en-aut-name=MasaiKaori
en-aut-sei=Masai
en-aut-mei=Kaori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakayamaYuta
en-aut-sei=Nakayama
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ShinKotaro
en-aut-sei=Shin
en-aut-mei=Kotaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SugaharaChiaki
en-aut-sei=Sugahara
en-aut-mei=Chiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YasuharaTakao
en-aut-sei=Yasuhara
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=DateIsao
en-aut-sei=Date
en-aut-mei=Isao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Medical Neurobiology, Okayama University Medical School
kn-affil=

affil-num=3
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Streptozotocin
kn-keyword=Streptozotocin
en-keyword=Adult neurogenesis
kn-keyword=Adult neurogenesis
en-keyword=Astrocyte
kn-keyword=Astrocyte
en-keyword=Microglia
kn-keyword=Microglia
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=1
article-no=
start-page=2926
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Large-volume focus control at 10 MHz refresh rate via fast line-scanning amplitude-encoded scattering-assisted holography
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The capability of focus control has been central to optical technologies that require both high temporal and spatial resolutions. However, existing varifocal lens schemes are commonly limited to the response time on the microsecond timescale and share the fundamental trade-off between the response time and the tuning power. Here, we propose an ultrafast holographic focusing method enabled by translating the speed of a fast 1D beam scanner into the speed of the complex wavefront modulation of a relatively slow 2D spatial light modulator. Using a pair of a digital micromirror device and a resonant scanner, we demonstrate an unprecedented refresh rate of focus control of 31?MHz, which is more than 1,000 times faster than the switching rate of a digital micromirror device. We also show that multiple micrometer-sized focal spots can be independently addressed in a range of over 1?MHz within a large volume of 5?mm �~ 5?mm �~ 5.5?mm, validating the superior spatiotemporal characteristics of the proposed technique ? high temporal and spatial precision, high tuning power, and random accessibility in a three-dimensional space. The demonstrated scheme offers a new route towards three-dimensional light manipulation in the 100?MHz regime.
en-copyright=
kn-copyright=

en-aut-name=ShibukawaAtsushi
en-aut-sei=Shibukawa
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HiguchiRyota
en-aut-sei=Higuchi
en-aut-mei=Ryota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SongGookho
en-aut-sei=Song
en-aut-mei=Gookho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MikamiHideharu
en-aut-sei=Mikami
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SudoYuki
en-aut-sei=Sudo
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JangMooseok
en-aut-sei=Jang
en-aut-mei=Mooseok
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Research Institute for Electronic Science, Hokkaido University
kn-affil=

affil-num=2
en-affil=Research Institute for Electronic Science, Hokkaido University
kn-affil=

affil-num=3
en-affil=Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology
kn-affil=

affil-num=4
en-affil=Research Institute for Electronic Science, Hokkaido University
kn-affil=

affil-num=5
en-affil=Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Bio and Brain Engineering, Korea Advanced Institute of Science and Technology
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=13
article-no=
start-page=6986
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240626
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Genome-Wide Association Study with Three Control Cohorts of Japanese Patients with Esotropia and Exotropia of Comitant Strabismus and Idiopathic Superior Oblique Muscle Palsy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Esotropia and exotropia in the entity of comitant strabismus are multifactorial diseases with both genetic and environmental backgrounds. Idiopathic superior oblique muscle palsy, as the predominant entity of non-comitant (paralytic) strabismus, also has a genetic background, as evidenced by varying degrees of muscle hypoplasia. A genome-wide association study (GWAS) was conducted of 711 Japanese patients with esotropia (n= 253), exotropia (n = 356), and idiopathic superior oblique muscle palsy (n = 102). The genotypes of single nucleotide polymorphisms (SNPs) were determined by Infinium Asian Screening Array. Three control cohorts from the Japanese population were used: two cohorts from BioBank Japan (BBJ) and the Nagahama Cohort. BBJ (180K) was genotyped by a different array, Illumina Infinium OmniExpressExome or HumanOmniExpress, while BBJ (ASA) and the Nagahama Cohort were genotyped by the same Asian array. After quality control of SNPs and individuals, common SNPs between the case cohort and the control cohort were chosen in the condition of genotyping by different arrays, while all SNPs genotyped by the same array were used for SNP imputation. The SNPs imputed with R-square values ? 0.3 were used to compare the case cohort of each entity or the combined entity with the control cohort. In comparison with BBJ (180K), the esotropia group and the exotropia group showed CDCA7 and HLA-F, respectively, as candidate genes at a significant level of p < 5 �~ 10?8, while the idiopathic superior oblique muscle palsy group showed DAB1 as a candidate gene which is involved in neuronal migration. DAB1 was also detected as a candidate in comparison with BBJ (ASA) and the Nagahama Cohort at a weak level of significance of p < 1 �~ 10?6. In comparison with BBJ (180K), RARB (retinoic acid receptor-��) was detected as a candidate at a significant level of p < 5 �~ 10?8 in the combined group of esotropia, exotropia, and idiopathic superior oblique muscle palsy. In conclusion, a series of GWASs with three different control cohorts would be an effective method with which to search for candidate genes for multifactorial diseases such as strabismus.
en-copyright=
kn-copyright=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HamasakiIchiro
en-aut-sei=Hamasaki
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KamataniYoichiro
en-aut-sei=Kamatani
en-aut-mei=Yoichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaguchiTakahisa
en-aut-sei=Kawaguchi
en-aut-mei=Takahisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamaguchiIzumi
en-aut-sei=Yamaguchi
en-aut-mei=Izumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=MatsudaFumihiko
en-aut-sei=Matsuda
en-aut-mei=Fumihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SaitoAkira
en-aut-sei=Saito
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakazonoKazuyuki
en-aut-sei=Nakazono
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=KamitsujiShigeo
en-aut-sei=Kamitsuji
en-aut-mei=Shigeo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Ophthalmology, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo
kn-affil=

affil-num=4
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=5
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=6
en-affil=Center for Genomic Medicine, Graduate School of Medicine, Kyoto University
kn-affil=

affil-num=7
en-affil=StaGen Co., Ltd.
kn-affil=

affil-num=8
en-affil=StaGen Co., Ltd.
kn-affil=

affil-num=9
en-affil=StaGen Co., Ltd.
kn-affil=
en-keyword=esotropia
kn-keyword=esotropia
en-keyword=exotropia
kn-keyword=exotropia
en-keyword=superior oblique muscle palsy
kn-keyword=superior oblique muscle palsy
en-keyword=genome-wide association study
kn-keyword=genome-wide association study
en-keyword=comitant strabismus
kn-keyword=comitant strabismus
en-keyword=non-comitant strabismus
kn-keyword=non-comitant strabismus
en-keyword=Japanese population
kn-keyword=Japanese population
en-keyword=BioBank Japan
kn-keyword=BioBank Japan
en-keyword=Nagahama Cohort
kn-keyword=Nagahama Cohort
en-keyword=Asian array
kn-keyword=Asian array
END

start-ver=1.4
cd-journal=joma
no-vol=41
cd-vols=
no-issue=3
article-no=
start-page=281
end-page=289
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Volume X-Ray Micro-Computed Tomography Analysis of the Early Cephalized Central Nervous System in a Marine Flatworm, Stylochoplana pusilla
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Platyhelminthes are a phylum of simple bilaterian invertebrates with prototypic body systems. Compared with non-bilaterians such as cnidarians, the bilaterians are likely to exhibit integrated free-moving behaviors, which require a concentrated nervous system �gbrain�h rather than the distributed nervous system of radiatans. Marine flatworms have an early cephalized �ecentral�f nervous system compared not only with non-bilaterians but also with parasitic flatworms or freshwater planarians. In this study, we used the marine flatworm Stylochoplana pusilla as an excellent model organism in Platyhelminthes because of the early cephalized central nervous system. Here, we investigated the three-dimensional structures of the flatworm central nervous system by the use of X-ray micro-computed tomography (micro-CT) in a synchrotron radiation facility. We found that the obtained tomographic images were sufficient to discriminate some characteristic structures of the nervous system, including nerve cords around the cephalic ganglion, mushroom body-like structures, and putative optic nerves forming an optic commissure-like structure. Through the micro-CT imaging, we could obtain undistorted serial section images, permitting us to visualize precise spatial relationships of neuronal subpopulations and nerve tracts. 3-D micro-CT is very effective in the volume analysis of the nervous system at the cellular level; the methodology is straightforward and could be applied to many other non-model organisms.
en-copyright=
kn-copyright=

en-aut-name=IkenagaTakanori
en-aut-sei=Ikenaga
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KobayashiAoshi
en-aut-sei=Kobayashi
en-aut-mei=Aoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TakeuchiAkihisa
en-aut-sei=Takeuchi
en-aut-mei=Akihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=UesugiKentaro
en-aut-sei=Uesugi
en-aut-mei=Kentaro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MaezawaTakanobu
en-aut-sei=Maezawa
en-aut-mei=Takanobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShibataNorito
en-aut-sei=Shibata
en-aut-mei=Norito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SakamotoTatsuya
en-aut-sei=Sakamoto
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Graduate School of Science and Engineering, Kagoshima University
kn-affil=

affil-num=2
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Japan Synchrotron Radiation Research Institute/SPring-8
kn-affil=

affil-num=4
en-affil=Japan Synchrotron Radiation Research Institute/SPring-8
kn-affil=

affil-num=5
en-affil=Department of Integrated Science and Technology, National Institute of Technology, Tsuyama College
kn-affil=

affil-num=6
en-affil=Department of Integrated Science and Technology, National Institute of Technology, Tsuyama College
kn-affil=

affil-num=7
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=8
en-affil=Ushimado Marine Institute (UMI), Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=bilaterians
kn-keyword=bilaterians
en-keyword=micro-CT scan
kn-keyword=micro-CT scan
en-keyword=central nervous system
kn-keyword=central nervous system
en-keyword=Platyhelminthes
kn-keyword=Platyhelminthes
en-keyword=marine flatworms
kn-keyword=marine flatworms
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=3
article-no=
start-page=276
end-page=281
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202405
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Postnatal longitudinal analysis of serum nitric oxide and eosinophil counts in extremely preterm infants
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Nitric oxide (NO) may be related to the pathogenesis of several morbidities in extremely preterm infants, including late-onset adrenal insufficiency. However, eosinophilia is observed under pathological conditions with adrenal insufficiency. Therefore, this study explored postnatal changes in NO levels and eosinophil counts in extremely preterm infants with and without morbidities.<br>
Methods: Nineteen extremely preterm infants with a median gestational age of 27.0 weeks and median birth weight of 888 g were enrolled in this study. Serum levels of nitrogen oxides (NOx) and peripheral blood eosinophil counts were measured at birth and every 2 weeks thereafter. Morbidities of the study group were diagnosed using a single criterion.<br>
Results: Serum NOx levels (mean �} standard deviation) were 22.5 �} 14.9 ��mol/L, 51.2 �} 23.7 ��mol/L, 42.4 �} 15.2 ��mol/L, and 33.8 �} 9.4 ��mol/L at birth and 2, 4, and 6 weeks of age, respectively. The serum NOx level at 2 weeks of age was significantly higher than that at birth and 6 weeks of age. Eosinophil counts, which increase with adrenal insufficiency, were measured simultaneously and were 145 �} 199/��L, 613 �} 625/��L, 466 �} 375/��L, and 292 �} 228/��L at birth and 2, 4, and 6 weeks of age, respectively. These values showed that the eosinophil count was significantly higher at 2 weeks of age than at birth and 6 weeks of age. The serum NOx level of infants without chorioamnionitis was significantly increased at 4 weeks of age, and the eosinophil count of infants with necrotizing enterocolitis was significantly increased at 2 weeks of age. No correlation with the NOx level or eosinophil count was observed in infants with late-onset circulatory collapse.<br>
Conclusion: The postnatal serum NOx level and eosinophil count were significantly correlated with each other and peaked at 2 weeks of age.
en-copyright=
kn-copyright=

en-aut-name=WatanabeHirokazu
en-aut-sei=Watanabe
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WashioYosuke
en-aut-sei=Washio
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TamaiKei
en-aut-sei=Tamai
en-aut-mei=Kei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MorimotoDaisaku
en-aut-sei=Morimoto
en-aut-mei=Daisaku
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkamuraTomoka
en-aut-sei=Okamura
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YoshimotoJunko
en-aut-sei=Yoshimoto
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakanishiHidehiko
en-aut-sei=Nakanishi
en-aut-mei=Hidehiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KageyamaMisao
en-aut-sei=Kageyama
en-aut-mei=Misao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=UchiyamaAtsushi
en-aut-sei=Uchiyama
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=KusudaSatoshi
en-aut-sei=Kusuda
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neonatology, Okayama Medical Center, National Hospital Organization
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women�fs Medical University
kn-affil=

affil-num=8
en-affil=Department of Neonatology, Okayama Medical Center, National Hospital Organization
kn-affil=

affil-num=9
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women�fs Medical University
kn-affil=

affil-num=10
en-affil=Department of Pediatrics, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Neonatology, Maternal and Perinatal Center, Tokyo Women�fs Medical University
kn-affil=
en-keyword=eosinophils
kn-keyword=eosinophils
en-keyword=extremely preterm infant
kn-keyword=extremely preterm infant
en-keyword=nitric oxide
kn-keyword=nitric oxide
en-keyword=relative adrenal insufficiency
kn-keyword=relative adrenal insufficiency
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=11
article-no=
start-page=5889
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240528
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Anti-HMGB1 mAb Therapy Reduces Epidural Hematoma Injury
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epidural and subdural hematomas are commonly associated with traumatic brain injury. While surgical removal is the primary intervention for these hematomas, it is also critical to prevent and reduce complications such as post-traumatic epilepsy, which may result from inflammatory responses in the injured brain areas. In the present study, we observed that high mobility group box-1 (HMGB1) decreased in the injured brain area beneath the epidural hematoma (EDH) in rats, concurrent with elevated plasma levels of HMGB1. Anti-HMGB1 monoclonal antibody therapy strongly inhibited both HMGB1 release and the subsequent increase in plasma levels. Moreover, this treatment suppressed the up-regulation of inflammatory cytokines and related molecules such as interleukin-1-beta (IL-1��), tumor necrosis factor-alpha (TNF-��), and inducible nitric oxide synthase (iNOS) in the injured areas. Our in vitro experiments using SH-SY5Y demonstrated that hematoma components?thrombin, heme, and ferrous ion? prompted HMGB1 translocation from the nuclei to the cytoplasm, a process inhibited by the addition of the anti-HMGB1 mAb. These findings suggest that anti-HMGB1 mAb treatment not only inhibits HMGB1 translocation but also curtails inflammation in injured areas, thereby protecting the neural tissue. Thus, anti-HMGB1 mAb therapy could serve as a complementary therapy for an EDH before/after surgery.
en-copyright=
kn-copyright=

en-aut-name=GaoShangze
en-aut-sei=Gao
en-aut-mei=Shangze
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=WangDengli
en-aut-sei=Wang
en-aut-mei=Dengli
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuKeyue
en-aut-sei=Liu
en-aut-mei=Keyue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonoYasuko
en-aut-sei=Tomono
en-aut-mei=Yasuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FuLi
en-aut-sei=Fu
en-aut-mei=Li
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=GaoYuan
en-aut-sei=Gao
en-aut-mei=Yuan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakahashiYohei
en-aut-sei=Takahashi
en-aut-mei=Yohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YataMariko
en-aut-sei=Yata
en-aut-mei=Mariko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Translational Research & Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=epidural hematoma
kn-keyword=epidural hematoma
en-keyword=HMGB1
kn-keyword=HMGB1
en-keyword=inflammatory response
kn-keyword=inflammatory response
END

start-ver=1.4
cd-journal=joma
no-vol=2024
cd-vols=
no-issue=
article-no=
start-page=6505595
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240528
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Circadian Rhythms Fluctuate the Treatment Effects of Intravesical Treatments on Rat Urinary Frequency Models
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Objectives. It is still not clear how the intravesical instillation of drugs affects rat urinary frequency. This study aimed to examine the dynamics of intravesical treatments' treatment effect on rat urinary frequency models by real-time and extended monitoring using a novel continuous urination monitoring system. Methods. Nine eleven-week-old female Wistar rats were divided into three groups to receive intravesical instillation of 0.1% acetic acid (AA), 1.0% AA, or phosphate-buffered saline (PBS). Thirty minutes later, these drugs were voided, and rats were moved to a continuous urination monitoring system, UM-100. UM-100 monitored rat urination quantitatively and continuously for 24 hours. Rats were then euthanized, and histopathologic examinations using a damage score validated the severity of bladder inflammation. We used nine additional rats to determine the treatment effect of various drugs against the urinary frequency. These rats were also treated with 1.0% AA in the same way and divided into three groups (n = 3 each) to receive intravesical instillation of lidocaine, silver nitrate (AgNO3), or dimethyl sulfoxide (DMSO), respectively. Thirty minutes later, rats were catheterized again and moved to the UM-100, and their voiding was monitored for 24 hours. Results. Intravesical instillation of AA increased the urinary frequency and decreased the mean voided volume (VV) in a concentration-dependent manner, with statistical significance at a concentration of 1.0% (urinary frequency; p = 0.0007 , mean VV; p = 0.0032 , respectively) compared with PBS. Histopathological analysis of these models demonstrated a significantly higher damage score of bladder mucosa in both 0.1% AA and 1.0% AA compared with PBS, with the severity in concordance with the clinical severity of urinary frequency (0.1% AA: p < 0.0001 , 1.0% AA: p < 0.0001 ). Moreover, intravesical instillation of lidocaine, AgNO3, and DMSO decreased the urinary frequency. Continuous monitoring with UM-100 also demonstrated that the treatment effect of these intravesically instilled drugs occurred only at night. Conclusions. The extended monitoring of rat urination by UM-100 revealed a significant fluctuation in the treatment effect of intravesically instilled drugs between day and night. These findings may help establish novel therapies for urinary frequency.
en-copyright=
kn-copyright=

en-aut-name=WatanabeTomofumi
en-aut-sei=Watanabe
en-aut-mei=Tomofumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SadahiraTakuya
en-aut-sei=Sadahira
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TominagaYusuke
en-aut-sei=Tominaga
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MaruyamaYuki
en-aut-sei=Maruyama
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NagasakiNaoya
en-aut-sei=Nagasaki
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SekitoTakanori
en-aut-sei=Sekito
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=EdamuraKohei
en-aut-sei=Edamura
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=WatanabeToyohiko
en-aut-sei=Watanabe
en-aut-mei=Toyohiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ArakiMotoo
en-aut-sei=Araki
en-aut-mei=Motoo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=WatanabeMasami
en-aut-sei=Watanabe
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=259
end-page=270
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Role of the Lipid Profile and Oxidative Stress in Fatigue, Sleep Disorders and Cognitive Impairment in Patients with Multiple Sclerosis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The aim of this study is to investigate the relationship of the lipid profile, dysfunctional high-density lipoprotein, ischaemia-modified albumin and thiol?disulfide homeostasis with cognitive impairment, fatigue and sleep disorders in patients with multiple sclerosis. The cognitive functions of patients were evaluated with the Brief International Cognitive Assessment for Multiple Sclerosis battery. Fatigue was evaluated with the Fatigue Severity Scale and the Fatigue Impact Scale. The Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale were used to assess patients�f sleep disturbance. Peripheral blood samples were collected, and lipid levels and myeloperoxidase and paraoxonase activity were measured. The myeloperoxidase/paraoxonase ratio, which indicates dysfunctional high-density lipoprotein, was calculated. Thiol?disulfide homeostasis and ischaemia-modified albumin were measured.<br>
We did not identify any relationship between dysfunctional high-density lipoprotein and the physical disability, cognitive decline, fatigue and sleep problems of multiple sclerosis. Thiol?disulfide homeostasis was associated with cognitive scores. The shift of the balance towards disulfide was accompanied by a decrease in cognitive scores. On the other hand, we did not detect any relationship between fatigue and sleep disorders and thiol?disulfide homeostasis. Our findings revealed a possible correlation between cognitive dysfunction and thiol?disulfide homeostasis in multiple sclerosis patients.
en-copyright=
kn-copyright=

en-aut-name=VuralGonul
en-aut-sei=Vural
en-aut-mei=Gonul
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DemirEsra
en-aut-sei=Demir
en-aut-mei=Esra
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=GumusyaylaSadiye
en-aut-sei=Gumusyayla
en-aut-mei=Sadiye
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ErenFunda
en-aut-sei=Eren
en-aut-mei=Funda
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BarakliSerdar
en-aut-sei=Barakli
en-aut-mei=Serdar
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NeseliogluSalim
en-aut-sei=Neselioglu
en-aut-mei=Salim
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ErelOzcan
en-aut-sei=Erel
en-aut-mei=Ozcan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Neurology, Faculty of Medicine, Ankara Yildirim Beyazit University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Ankara City Hospital
kn-affil=

affil-num=3
en-affil=Department of Neurology, Faculty of Medicine, Ankara Yildirim Beyazit University
kn-affil=

affil-num=4
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=

affil-num=5
en-affil=Department of Neurology, Ankara City Hospital
kn-affil=

affil-num=6
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=

affil-num=7
en-affil=Department of Clinical Biochemistry, Ankara City Hospital
kn-affil=
en-keyword=multiple sclerosis
kn-keyword=multiple sclerosis
en-keyword=dysfunctional HDL
kn-keyword=dysfunctional HDL
en-keyword=thiol?disulfide homeostasis
kn-keyword=thiol?disulfide homeostasis
en-keyword=cognitive decline
kn-keyword=cognitive decline
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=3
article-no=
start-page=227
end-page=235
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202406
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Effect of Lipopolysaccharide on the Duration of Zolpidem-Induced Loss of Righting Reflex in Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Zolpidem, a non-benzodiazepine hypnotic, is primarily used to treat insomnia. In a previous study, pior treatment with non-benzodiazepine receptor agonists was associated with inflammation. The present study aimed to clarify the association between the effects of zolpidem and inflammation in mice treated with lipopolysaccharide (LPS), a known model of inflammation. We assessed the zolpidem-induced loss of righting reflex (LORR) duration 24 h after LPS treatment in mice. Additionally, the expressions of ��-aminobutyric acid (GABA)A receptor subunit and K+-Cl? cotransporter isoform 2 (KCC2) mRNA in the hippocampus and frontal cortex were examined in LPS-treated mice. Pretreatment with LPS was associated with significantly prolonged duration of zolpidem-induced LORR compared to control mice. This effect was significantly attenuated by administering bicuculline, a GABAA receptor antagonist, or flumazenil, a benzodiazepine receptor antagonist, in LPS-treated mice. Compared to controls, LPS-treated mice showed no significant change in the expression of GABAA receptor subunits in the hippocampus or frontal cortex. Bumetanide, an Na+-K+-2Cl? cotransporter isoform 1 blocker, attenuated the extended duration of zolpidem-induced LORR observed in LPS-treated mice. LPS significantly decreased Kcc2 mRNA expression in the hippocampus and the frontal cortex. These findings suggest that inflammation increases zolpidem-induced LORR, possibly through a reduction in KCC2 expression.
en-copyright=
kn-copyright=

en-aut-name=WadaYudai
en-aut-sei=Wada
en-aut-mei=Yudai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=UshioSoichiro
en-aut-sei=Ushio
en-aut-mei=Soichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ZamamiYoshito
en-aut-sei=Zamami
en-aut-mei=Yoshito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Clinical Pharmacy, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Clinical Pharmacy, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Clinical Pharmacy, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Clinical Pharmacy, Okayama University, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=lipopolysaccharide
kn-keyword=lipopolysaccharide
en-keyword=zolpidem
kn-keyword=zolpidem
en-keyword=GABAA receptor
kn-keyword=GABAA receptor
en-keyword=K+-Cl? cotransporters
kn-keyword=K+-Cl? cotransporters
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=5
article-no=
start-page=e0302537
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240521
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The use of artificial intelligence in induced pluripotent stem cell-based technology over 10-year period: A systematic scoping review
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background <br>
Stem cell research, particularly in the domain of induced pluripotent stem cell (iPSC) technology, has shown significant progress. The integration of artificial intelligence (AI), especially machine learning (ML) and deep learning (DL), has played a pivotal role in refining iPSC classification, monitoring cell functionality, and conducting genetic analysis. These enhancements are broadening the applications of iPSC technology in disease modelling, drug screening, and regenerative medicine. This review aims to explore the role of AI in the advancement of iPSC research.<br>
Methods <br>
In December 2023, data were collected from three electronic databases (PubMed, Web of Science, and Science Direct) to investigate the application of AI technology in iPSC processing.<br>
Results <br>
This systematic scoping review encompassed 79 studies that met the inclusion criteria. The number of research studies in this area has increased over time, with the United States emerging as a leading contributor in this field. AI technologies have been diversely applied in iPSC technology, encompassing the classification of cell types, assessment of disease-specific phenotypes in iPSC-derived cells, and the facilitation of drug screening using iPSC. The precision of AI methodologies has improved significantly in recent years, creating a foundation for future advancements in iPSC-based technologies.<br>
Conclusions <br>
Our review offers insights into the role of AI in regenerative and personalized medicine, highlighting both challenges and opportunities. Although still in its early stages, AI technologies show significant promise in advancing our understanding of disease progression and development, paving the way for future clinical applications.
en-copyright=
kn-copyright=

en-aut-name=VoQuan Duy
en-aut-sei=Vo
en-aut-mei=Quan Duy
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoYukihiro
en-aut-sei=Saito
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IdaToshihiro
en-aut-sei=Ida
en-aut-mei=Toshihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraKazufumi
en-aut-sei=Nakamura
en-aut-mei=Kazufumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YuasaShinsuke
en-aut-sei=Yuasa
en-aut-mei=Shinsuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cardiovascular Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Faculty of Medicine, Department of Cardiovascular Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=13
end-page=18
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240526
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Application of a Deep Reinforcement Learning Algorithm to Virtual Machine Migration Control in Multi-Stage Information Processing Systems
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=This paper tackles a Virtual Machine (VM) migration control problem to maximize the progress (accuracy) of information processing tasks in multi-stage information processing systems. The conventional methods for this problem (e.g., VM sweeping method and VM number averaging method) are effective only for specific situations, such as when the system load is high. In this paper, in order to achieve high accuracy in various situations, we propose a VM migration method using a Deep Reinforcement Learning (DRL) algorithm. It is difficult to directly apply a DRL algorithm to the VM migration control problem because the size of the solution space of the problem dynamically changes according to the number of VMs staying in the system while the size of the agent�fs action space is fixed in DRL algorithms. Therefore, the proposed method divides the VM migration control problem into two problems: the problem of determining only the VM distribution (i.e., the proportion of the number of VMs deployed on each edge server) and the problem of determining the locations of all the VMs so that it follows the determined VM distribution. The former problem is solved by a DRL algorithm, and the latter problem is solved by a heuristic method. The simulation results confirm that our proposed method can select quasi-optimal VM locations in various situations with different link delays.
en-copyright=
kn-copyright=

en-aut-name=FukushimaYukinobu
en-aut-sei=Fukushima
en-aut-mei=Yukinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KoujitaniYuki
en-aut-sei=Koujitani
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NakaneKazutoshi
en-aut-sei=Nakane
en-aut-mei=Kazutoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TarutaniYuta
en-aut-sei=Tarutani
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=WuCelimuge
en-aut-sei=Wu
en-aut-mei=Celimuge
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=JiYusheng
en-aut-sei=Ji
en-aut-mei=Yusheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YokohiraTokumi
en-aut-sei=Yokohira
en-aut-mei=Tokumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MuraseTutomu
en-aut-sei=Murase
en-aut-mei=Tutomu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Okayama University
kn-affil=

affil-num=2
en-affil=Okayama University
kn-affil=

affil-num=3
en-affil=Nagoya University
kn-affil=

affil-num=4
en-affil=Okayama University
kn-affil=

affil-num=5
en-affil=The Univ. of Electro-Commun.
kn-affil=

affil-num=6
en-affil=National Institute of Informatics
kn-affil=

affil-num=7
en-affil=Okayama University
kn-affil=

affil-num=8
en-affil=Nagoya University
kn-affil=
en-keyword=Multi-stage information processing system
kn-keyword=Multi-stage information processing system
en-keyword=VM migration control
kn-keyword=VM migration control
en-keyword=Deep reinforcement learning
kn-keyword=Deep reinforcement learning
en-keyword=Deep Deterministic Policy Gradient (DDPG)
kn-keyword=Deep Deterministic Policy Gradient (DDPG)
END

start-ver=1.4
cd-journal=joma
no-vol=391
cd-vols=
no-issue=2
article-no=
start-page=249
end-page=267
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20221122
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The medaka mutant deficient in eyes shut homolog exhibits opsin transport defects and enhanced autophagy in retinal photoreceptors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Eyes shut homolog (EYS) encodes a proteoglycan and the human mutation causes retinitis pigmentosa type 25 (RP25) with progressive retinal degeneration. RP25 most frequently affects autosomal recessive RP patients with many ethnic backgrounds. Although studies using RP models have facilitated the development of therapeutic medications, Eys has been lost in rodent model animals. Here we examined the roles for Eys in the maintenance of photoreceptor structure and function by generating eys-null medaka fish using the CRISPR-Cas9 system. Medaka EYS protein was present near the connecting cilium of wild-type photoreceptors, while it was absent from the eys?/? retina. The mutant larvae exhibited a reduced visual motor response compared with wild-type. In contrast to reported eys-deficient zebrafish at the similar stage, no retinal cell death was detected in the 8-month post-hatching (8-mph) medaka eys mutant. Immunohistochemistry showed a significant reduction in the length of cone outer segments (OSs), retention of OS proteins in the inner segments of photoreceptors, and abnormal filamentous actin network at the base of cone OSs in the mutant retina by 8 mph. Electron microscopy revealed aberrant structure of calyceal processes, numerous vesiculation and lamellar interruptions, and autophagosomes in the eys-mutant cone photoreceptors. In situ hybridization showed an autophagy component gene, gabarap, was ectopically expressed in the eys-null retina. These results suggest eys is required for regeneration of OS, especially of cone photoreceptors, and transport of OS proteins by regulating actin filaments. Enhanced autophagy may delay the progression of retinal degeneration when lacking EYS in the medaka retina.
en-copyright=
kn-copyright=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=LiuYang
en-aut-sei=Liu
en-aut-mei=Yang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamashitaTakahiro
en-aut-sei=Yamashita
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
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affil-num=1
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affil-num=2
en-affil=Department of Cytology and Histology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
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affil-num=3
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affil-num=4
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en-title=ASL �B�e���ł��Ȃ� MRI ���u�ɂ�����ĔR���̔]��������𔺂����� MELAS ��ΏۂƂ��� FLAIR �摜��p�����f�f�̒��
kn-title=Proposal for diagnosis using FLAIR image aimed for pediatric MELAS with recurrent stroke-like episodes on MRI system cannot take ASL imaging.
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en-aut-name=SAKAGAMITosuke
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affil-num=1
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kn-title=A Study on Efficient Methods for Optimal Design and Countermeasures Using Equivalent Circuit Models to Satisfy EMC Performance in Multi-Component Systems
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kn-title=Enhancing E-Learning Efficiency: A Comprehensive Approach for Computer-Aided Rote Learning through Automated Deck Generation and Audio Reinforcement
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en-aut-name=MORIMOTOAtsushi
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en-aut-name=ADACHIReimi
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affil-num=1
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en-title=CRISPR/dCas13�����RNA�Ɖu���~�ɂ��SARS-CoV-2 5�fUTR RNA�ƃq�g������ӌo�H�Ƃ̑��ݍ�p�����炩�ƂȂ�
kn-title=An RNA-immunoprecipitation via CRISPR/dCas13 reveals an interaction between the SARS-CoV-2 5'UTR RNA and the process of human lipid metabolism
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en-aut-name=SHIMIZUYurika
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affil-num=1
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kn-title=Interaction of Orexin and Bone Morphogenetic Proteins in Steroidogenesis by Human Adrenocortical Cells
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en-aut-name=SOEJIMAYoshiaki
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affil-num=1
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en-title=�]���s�f���ɂ�鐳�����ˏ������Ԃɑ΂���LPS�̉e���ɂ���
kn-title=Effect of Lipopolysaccharide on the Duration of Zolpidem-Induced Loss of Righting Reflex in Mice
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en-aut-name=WADAYudai
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affil-num=1
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END

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en-title=�����g�D�^�얞�זE��Noradrenaline�𒙑��A���o����
kn-title=Connective tissue mast cells store and release noradrenaline
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en-aut-name=OTANIYusuke
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en-aut-mei=Yusuke
kn-aut-name=��J�I��
kn-aut-sei=��J
kn-aut-mei=�I��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

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en-title=�����Y���ɂ����錌����_�����f�ƍD�_���̏o����̏c�f�I���
kn-title=Postnatal longitudinal analysis of serum nitric oxide and eosinophil counts in extremely preterm infants
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kn-subtitle=
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kn-copyright=

en-aut-name=WATANABEHirokazu
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en-aut-mei=Hirokazu
kn-aut-name=�n糍G�a
kn-aut-sei=�n�
kn-aut-mei=�G�a
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

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cd-vols=
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dt-received=
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kn-subject=
en-title=�}�E�X�n���ɂ���ĈقȂ�ϊ������n����ES�זE�ɂ����Ă����݂���
kn-title=Mouse embryonic stem cells embody organismal-level cold resistance
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kn-subtitle=
en-abstract=
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kn-copyright=

en-aut-name=SUITAKoukyou
en-aut-sei=SUITA
en-aut-mei=Koukyou
kn-aut-name=���c�W��
kn-aut-sei=���c
kn-aut-mei=�W��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

start-ver=1.4
cd-journal=joma
no-vol=57
cd-vols=
no-issue=2
article-no=
start-page=85
end-page=88
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240425
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kn-subject=
en-title=
kn-title=Membrane-Targeted palGFP Predominantly Localizes to the Plasma Membrane but not to Neurosecretory Vesicle Membranes in Rat Oxytocin Neurons
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Recent advances in viral vector technology, specifically using adeno-associated virus (AAV) vectors, have significantly expanded possibilities in neuronal tracing. We have utilized the Cre/loxP system in combination with AAV techniques in rats to explore the subcellular localization of palmitoylation signal-tagged GFP (palGFP) in oxytocin-producing neurosecretory neurons. A distinctive branching pattern of single axons was observed at the level of the terminals in the posterior pituitary. Despite challenges in detecting palGFP signals by fluorescent microscopy, immunoelectron microscopy demonstrated predominant localization on the plasma membrane, with a minor presence on the neurosecretory vesicle membrane. These findings suggest that membrane-anchored palGFP may undergo exocytosis, translocating from the plasma membrane to the neurosecretory vesicle membrane. In this study, we observed characteristic axon terminal structures in the posterior pituitary of oxytocin neurons. This study indicates the importance of understanding the plasma membrane-specific sorting system in neuronal membrane migration and encourages future studies on the underlying mechanisms.
en-copyright=
kn-copyright=

en-aut-name=SakamotoHirotaka
en-aut-sei=Sakamoto
en-aut-mei=Hirotaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=InutsukaAyumu
en-aut-sei=Inutsuka
en-aut-mei=Ayumu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Biology, Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Division of Brain and Neurophysiology, Department of Physiology, Jichi Medical University
kn-affil=
en-keyword=GFP with a palmitoylation signal (palGFP)
kn-keyword=GFP with a palmitoylation signal (palGFP)
en-keyword=plasmalemma localization
kn-keyword=plasmalemma localization
en-keyword=neurosecretory vesicle
kn-keyword=neurosecretory vesicle
en-keyword=immunoelectron microscopy
kn-keyword=immunoelectron microscopy
en-keyword=oxytocin
kn-keyword=oxytocin
END

start-ver=1.4
cd-journal=joma
no-vol=1828
cd-vols=
no-issue=
article-no=
start-page=148790
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protective effect of scallop-derived plasmalogen against vascular dysfunction, via the pSTAT3/PIM1/NFATc1 axis, in a novel mouse model of Alzheimer�fs disease with cerebral hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A strong relationship between Alzheimer�fs disease (AD) and vascular dysfunction has been the focus of increasing attention in aging societies. In the present study, we examined the long-term effect of scallop-derived plasmalogen (sPlas) on vascular remodeling-related proteins in the brain of an AD with cerebral hypoperfusion (HP) mouse model. We demonstrated, for the first time, that cerebral HP activated the axis of the receptor for advanced glycation endproducts (RAGE)/phosphorylated signal transducer and activator of transcription 3 (pSTAT3)/provirus integration site for Moloney murine leukemia virus 1 (PIM1)/nuclear factor of activated T cells 1 (NFATc1), accounting for such cerebral vascular remodeling. Moreover, we also found that cerebral HP accelerated pSTAT3-mediated astrogliosis and activation of the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome, probably leading to cognitive decline. On the other hand, sPlas treatment attenuated the activation of the pSTAT3/PIM1/NFATc1 axis independent of RAGE and significantly suppressed NLRP3 inflammasome activation, demonstrating the beneficial effect on AD.
en-copyright=
kn-copyright=

en-aut-name=ZhaiYun
en-aut-sei=Zhai
en-aut-mei=Yun
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriharaRyuta
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en-aut-mei=Ryuta
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kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FengTian
en-aut-sei=Feng
en-aut-mei=Tian
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kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
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kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=FukuiYusuke
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en-aut-mei=Yusuke
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kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=BianZhihong
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aut-affil-num=6
ORCID=

en-aut-name=BianYuting
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en-aut-mei=Yuting
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kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YuHaibo
en-aut-sei=Yu
en-aut-mei=Haibo
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kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakemotoMami
en-aut-sei=Takemoto
en-aut-mei=Mami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=TangYing
en-aut-sei=Tang
en-aut-mei=Ying
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=11
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=12
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=13
en-affil=Department of Neurology, The First Affiliated Hospital of Harbin Medical University
kn-affil=

affil-num=14
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=15
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer's disease
kn-keyword=Alzheimer's disease
en-keyword=Hypoperfusion
kn-keyword=Hypoperfusion
en-keyword=Cerebral vascular remodeling
kn-keyword=Cerebral vascular remodeling
en-keyword=Scallop-derived plasmalogen
kn-keyword=Scallop-derived plasmalogen
en-keyword=pSTAT3/PIM1/NFATc1 axis
kn-keyword=pSTAT3/PIM1/NFATc1 axis
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230523
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A four-oscillator model of seasonally adapted morning and evening activities in Drosophila melanogaster
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The fruit fly Drosophila melanogaster exhibits two activity peaks, one in the morning and another in the evening. Because the two peaks change phase depending on the photoperiod they are exposed to, they are convenient for studying responses of the circadian clock to seasonal changes. To explain the phase determination of the two peaks, Drosophila researchers have employed the two-oscillator model, in which two oscillators control the two peaks. The two oscillators reside in different subsets of neurons in the brain, which express clock genes, the so-called clock neurons. However, the mechanism underlying the activity of the two peaks is complex and requires a new model for mechanistic exploration. Here, we hypothesize a four-oscillator model that controls the bimodal rhythms. The four oscillators that reside in different clock neurons regulate activity in the morning and evening and sleep during the midday and at night. In this way, bimodal rhythms are formed by interactions among the four oscillators (two activity and two sleep oscillators), which may judiciously explain the flexible waveform of activity rhythms under different photoperiod conditions. Although still hypothetical, this model would provide a new perspective on the seasonal adaptation of the two activity peaks.
en-copyright=
kn-copyright=

en-aut-name=YoshiiTaishi
en-aut-sei=Yoshii
en-aut-mei=Taishi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=SaitoAika
en-aut-sei=Saito
en-aut-mei=Aika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YokosakoTatsuya
en-aut-sei=Yokosako
en-aut-mei=Tatsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Drosophila
kn-keyword=Drosophila
en-keyword=Seasonal adaptation
kn-keyword=Seasonal adaptation
en-keyword=Photoperiod
kn-keyword=Photoperiod
en-keyword=Oscillator
kn-keyword=Oscillator
en-keyword=Activity rhythm
kn-keyword=Activity rhythm
END

start-ver=1.4
cd-journal=joma
no-vol=174
cd-vols=
no-issue=5
article-no=
start-page=451
end-page=459
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Direct binding of calmodulin to the cytosolic C-terminal regions of sweet/umami taste receptors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sweet and umami taste receptors recognize chemicals such as sugars and amino acids on their extracellular side and transmit signals into the cytosol of the taste cell. In contrast to ligands that act on the extracellular side of these receptors, little is known regarding the molecules that regulate receptor functions within the cytosol. In this study, we analysed the interaction between sweet and umami taste receptors and calmodulin, a representative Ca2+-dependent cytosolic regulatory protein. High prediction scores for calmodulin binding were observed on the C-terminal cytosolic side of mouse taste receptor type 1 subunit 3 (T1r3), a subunit that is common to both sweet and umami taste receptors. Pull-down assay and surface plasmon resonance analyses showed different affinities of calmodulin to the C-terminal tails of distinct T1r subtypes. Furthermore, we found that T1r3 and T1r2 showed the highest and considerable binding to calmodulin, whereas T1r1 showed weaker binding affinity. Finally, the binding of calmodulin to T1rs was consistently higher in the presence of Ca2+ than in its absence. The results suggested a possibility of the Ca2+-dependent feedback regulation process of sweet and umami taste receptor signaling by calmodulin.
en-copyright=
kn-copyright=

en-aut-name=YoshidaAtsuki
en-aut-sei=Yoshida
en-aut-mei=Atsuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ItoAyumi
en-aut-sei=Ito
en-aut-mei=Ayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YasuiNorihisa
en-aut-sei=Yasui
en-aut-mei=Norihisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YamashitaAtsuko
en-aut-sei=Yamashita
en-aut-mei=Atsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=calmodulin
kn-keyword=calmodulin
en-keyword=cytosol
kn-keyword=cytosol
en-keyword=sweet taste
kn-keyword=sweet taste
en-keyword=taste receptor type 1
kn-keyword=taste receptor type 1
en-keyword=umami taste
kn-keyword=umami taste
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=7
article-no=
start-page=2333
end-page=2345
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240427
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Adrenergic microenvironment driven by cancer-associated Schwann cells contributes to chemoresistance in patients with lung cancer
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Doublecortin (DCX)-positive neural progenitor-like cells are purported components of the cancer microenvironment. The number of DCX-positive cells in tissues reportedly correlates with cancer progression; however, little is known about the mechanism by which these cells affect cancer progression. Here we demonstrated that DCX-positive cells, which are found in all major histological subtypes of lung cancer, are cancer-associated Schwann cells (CAS) and contribute to the chemoresistance of lung cancer cells by establishing an adrenergic microenvironment. Mechanistically, the activation of the Hippo transducer YAP/TAZ was involved in the acquisition of new traits of CAS and DCX positivity. We further revealed that CAS express catecholamine-synthesizing enzymes and synthesize adrenaline, which potentiates the chemoresistance of lung cancer cells through the activation of YAP/TAZ. Our findings shed light on CAS, which drive the formation of an adrenergic microenvironment by the reciprocal regulation of YAP/TAZ in lung cancer tissues.
en-copyright=
kn-copyright=

en-aut-name=OtaniYusuke
en-aut-sei=Otani
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatayamaHaruyoshi
en-aut-sei=Katayama
en-aut-mei=Haruyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=ZhuYidan
en-aut-sei=Zhu
en-aut-mei=Yidan
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HuangRongsheng
en-aut-sei=Huang
en-aut-mei=Rongsheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShigehiraTakafumi
en-aut-sei=Shigehira
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=ShienKazuhiko
en-aut-sei=Shien
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=SuzawaKen
en-aut-sei=Suzawa
en-aut-mei=Ken
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoHiromasa
en-aut-sei=Yamamoto
en-aut-mei=Hiromasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=ShienTadahiko
en-aut-sei=Shien
en-aut-mei=Tadahiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=ToyookaShinichi
en-aut-sei=Toyooka
en-aut-mei=Shinichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Trauma Orthopedics, The Second Hospital of Dalian Medical University
kn-affil=

affil-num=5
en-affil=Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and  Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=adrenaline
kn-keyword=adrenaline
en-keyword=cancer-associated Schwann cells
kn-keyword=cancer-associated Schwann cells
en-keyword=doublecortin
kn-keyword=doublecortin
en-keyword=microenvironment
kn-keyword=microenvironment
en-keyword=YAP/TAZ
kn-keyword=YAP/TAZ
END

start-ver=1.4
cd-journal=joma
no-vol=174
cd-vols=
no-issue=6
article-no=
start-page=533
end-page=548
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230919
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Phosphorylated SARM1 is involved in the pathological process of rotenone-induced neurodegeneration
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Sterile alpha and Toll/interleukin receptor motif-containing protein 1 (SARM1) is a NAD+ hydrolase that plays a key role in axonal degeneration and neuronal cell death. We reported that c-Jun N-terminal kinase (JNK) activates SARM1 through phosphorylation at Ser-548. The importance of SARM1 phosphorylation in the pathological process of Parkinson�fs disease (PD) has not been determined. We thus conducted the present study by using rotenone (an inducer of PD-like pathology) and neurons derived from induced pluripotent stem cells (iPSCs) from healthy donors and a patient with familial PD PARK2 (FPD2). The results showed that compared to the healthy neurons, FPD2 neurons were more vulnerable to rotenone-induced stress and had higher levels of SARM1 phosphorylation. Similar cellular events were obtained when we used PARK2-knockdown neurons derived from healthy donor iPSCs. These events in both types of PD-model neurons were suppressed in neurons treated with JNK inhibitors, Ca2+-signal inhibitors, or by a SARM1-knockdown procedure. The degenerative events were enhanced in neurons overexpressing wild-type SARM1 and conversely suppressed in neurons overexpressing the SARM1-S548A mutant. We also detected elevated SARM1 phosphorylation in the midbrain of PD-model mice. The results indicate that phosphorylated SARM1 plays an important role in the pathological process of rotenone-induced neurodegeneration.
en-copyright=
kn-copyright=

en-aut-name=MurataHitoshi
en-aut-sei=Murata
en-aut-mei=Hitoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=PhooMay Tha Zin
en-aut-sei=Phoo
en-aut-mei=May Tha Zin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OchiToshiki
en-aut-sei=Ochi
en-aut-mei=Toshiki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TomonobuNahoko
en-aut-sei=Tomonobu
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=YamamotoKen-ichi
en-aut-sei=Yamamoto
en-aut-mei=Ken-ichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KinoshitaRie
en-aut-sei=Kinoshita
en-aut-mei=Rie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MiyazakiIkuko
en-aut-sei=Miyazaki
en-aut-mei=Ikuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NishiboriMasahiro
en-aut-sei=Nishibori
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=AsanumaMasato
en-aut-sei=Asanuma
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Translational Research and Drug Development, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=JNK
kn-keyword=JNK
en-keyword=PARK2
kn-keyword=PARK2
en-keyword=Parkinson�fsdisease
kn-keyword=Parkinson�fsdisease
en-keyword=Phosphorylation
kn-keyword=Phosphorylation
en-keyword=SARM1
kn-keyword=SARM1
END

start-ver=1.4
cd-journal=joma
no-vol=68
cd-vols=
no-issue=3
article-no=
start-page=169
end-page=174
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230120
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Recent advances in CGG repeat diseases and a proposal of fragile X-associated tremor/ataxia syndrome, neuronal intranuclear inclusion disease, and oculophryngodistal myopathy (FNOP) spectrum disorder
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=While whole genome sequencing and long-read sequencing have become widely available, more and more focuses are on noncoding expanded repeats. Indeed, more than half of noncoding repeat expansions related to diseases have been identified in the five years. An exciting aspect of the progress in this field is an identification of a phenomenon called repeat motif?phenotype correlation. Repeat motif?phenotype correlation in noncoding repeat expansion diseases is first found in benign adult familial myoclonus epilepsy. The concept is extended in the research of CGG repeat expansion diseases. In this review, we focus on newly identified CGG repeat expansion diseases, update the concept of repeat motif?phenotype correlation in CGG repeat expansion diseases, and propose a clinical concept of FNOP (fragile X-associated tremor/ataxia syndrome, neuronal intranuclear inclusion disease, and oculopharyngodistal myopathy)-spectrum disorder, which shares clinical features and thus probably share some common disease pathophysiology, to further facilitate discussion and progress in this field.
en-copyright=
kn-copyright=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TsujiShoji
en-aut-sei=Tsuji
en-aut-mei=Shoji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TodaTatsushi
en-aut-sei=Toda
en-aut-mei=Tatsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=

affil-num=3
en-affil=Department of Neurology, Graduate School of Medicine, The University of Tokyo
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=2
article-no=
start-page=115
end-page=122
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Impacts of Age and Gender on Brain Edema in a Mouse Water Intoxication Model
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Brain edema causes abnormal fluid retention and can be fatal in severe cases. Although it develops in various diseases, most treatments for brain edema are classical. We analyzed the impacts of age and gender on the characteristics of a water intoxication model that induces pure brain edema in mice and examined the model�fs usefulness for research regarding new treatments for brain edema. C57BL/6J mice received an intraperitoneal administration of 10% body weight distilled water, and we calculated the brain water content by measuring the brain-tissue weight immediately after dissection and after drying. We analyzed 8-OHdG and caspase-3 values to investigate the brain damage. We also applied this model in aquaporin 4 knockout (AQP4?) mice and compared these mice with wild-type mice. The changes in water content differed by age and gender, and the 8-OHdG and caspase-3 values differed by age. Suppression of brain edema by AQP4? was also confirmed. These results clarified the differences in the onset of brain edema by age and gender, highlighting the importance of considering the age and gender of model animals. Similar studies using genetically modified mice are also possible. Our findings indicate that this water intoxication model is effective for explorations of new brain edema treatments.
en-copyright=
kn-copyright=

en-aut-name=Nakamura-MaruyamaEmi
en-aut-sei=Nakamura-Maruyama
en-aut-mei=Emi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IrieKeiichiro
en-aut-sei=Irie
en-aut-mei=Keiichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NaritaKazuhiko
en-aut-sei=Narita
en-aut-mei=Kazuhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HimiNaoyuki
en-aut-sei=Himi
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MiyamotoOsamu
en-aut-sei=Miyamoto
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakamuraTakehiro
en-aut-sei=Nakamura
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of Physiology2, Kawasaki Medical School
kn-affil=

affil-num=2
en-affil=Department of Neurological Surgery, Kagawa University Faculty of Medicine
kn-affil=

affil-num=3
en-affil=Department of Physiology2, Kawasaki Medical School
kn-affil=

affil-num=4
en-affil=Department of Physiology2, Kawasaki Medical School
kn-affil=

affil-num=5
en-affil=Department of Physiology2, Kawasaki Medical School
kn-affil=

affil-num=6
en-affil=Department of Physiology2, Kawasaki Medical School
kn-affil=
en-keyword=brain edema
kn-keyword=brain edema
en-keyword=water intoxication model
kn-keyword=water intoxication model
en-keyword=age
kn-keyword=age
en-keyword=gender
kn-keyword=gender
en-keyword=AQP4
kn-keyword=AQP4
END

start-ver=1.4
cd-journal=joma
no-vol=78
cd-vols=
no-issue=2
article-no=
start-page=95
end-page=106
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=The Roles of Neuropeptide Y in Respiratory Disease Pathogenesis via the Airway Immune Response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The lungs are very complex organs, and the respiratory system performs the dual roles of repairing tissue while protecting against infection from various environmental stimuli. Persistent external irritation disrupts the immune responses of tissues and cells in the respiratory system, ultimately leading to respiratory disease. Neuropeptide Y (NPY) is a 36-amino-acid polypeptide and a neurotransmitter that regulates homeostasis. The NPY receptor is a seven-transmembrane-domain G-protein-coupled receptor with six subtypes (Y1, Y2, Y3, Y4, Y5, and Y6). Of these receptors, Y1, Y2, Y4, and Y5 are functional in humans, and Y1 plays important roles in the immune responses of many organs, including the respiratory system. NPY and the Y1 receptor have critical roles in the pathogenesis of asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis. The effects of NPY on the airway immune response and pathogenesis differ among respiratory diseases. This review focuses on the involvement of NPY in the airway immune response and pathogenesis of various respiratory diseases.
en-copyright=
kn-copyright=

en-aut-name=ItanoJunko
en-aut-sei=Itano
en-aut-mei=Junko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MaedaYoshinobu
en-aut-sei=Maeda
en-aut-mei=Yoshinobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyaharaNobuaki
en-aut-sei=Miyahara
en-aut-mei=Nobuaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Hematology, Oncology and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Allergy and Respiratory Medicine, Okayama University Hospital
kn-affil=
en-keyword=neuropeptide y
kn-keyword=neuropeptide y
en-keyword=Y1 receptor
kn-keyword=Y1 receptor
en-keyword=airway immune response
kn-keyword=airway immune response
en-keyword=bronchial epithelial cells
kn-keyword=bronchial epithelial cells
en-keyword=respiratory disease
kn-keyword=respiratory disease
END

start-ver=1.4
cd-journal=joma
no-vol=14
cd-vols=
no-issue=1
article-no=
start-page=6723
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Development of a novel AAK1 inhibitor via Kinobeads-based screening
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A chemical proteomics approach using Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) inhibitor-immobilized sepharose (TIM-063-Kinobeads) identified main targets such as CaMKK alpha/1 and beta/2, and potential off-target kinases, including AP2-associated protein kinase 1 (AAK1), as TIM-063 interactants. Because TIM-063 interacted with the AAK1 catalytic domain and inhibited its enzymatic activity moderately (IC50 = 8.51 mu M), we attempted to identify potential AAK1 inhibitors from TIM-063-derivatives and found a novel AAK1 inhibitor, TIM-098a (11-amino-2-hydroxy-7H-benzo[de]benzo[4,5]imidazo[2,1-a]isoquinolin-7-one) which is more potent (IC50 = 0.24 mu M) than TIM-063 without any inhibitory activity against CaMKK isoforms and a relative AAK1-selectivity among the Numb-associated kinases family. TIM-098a could inhibit AAK1 activity in transfected cultured cells (IC50 = 0.87 mu M), indicating cell-membrane permeability of the compound. Overexpression of AAK1 in HeLa cells significantly reduced the number of early endosomes, which was blocked by treatment with 10 mu M TIM-098a. These results indicate TIM-063-Kinobeads-based chemical proteomics is efficient for identifying off-target kinases and re-evaluating the kinase inhibitor (TIM-063), leading to the successful development of a novel inhibitory compound (TIM-098a) for AAK1, which could be a molecular probe for AAK1. TIM-098a may be a promising lead compound for a more potent, selective and therapeutically useful AAK1 inhibitor.
en-copyright=
kn-copyright=

en-aut-name=YoshidaAkari
en-aut-sei=Yoshida
en-aut-mei=Akari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhtsukaSatomi
en-aut-sei=Ohtsuka
en-aut-mei=Satomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsumotoFumiya
en-aut-sei=Matsumoto
en-aut-mei=Fumiya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyagawaTomoyuki
en-aut-sei=Miyagawa
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OkinoRei
en-aut-sei=Okino
en-aut-mei=Rei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=IkedaYumeya
en-aut-sei=Ikeda
en-aut-mei=Yumeya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TadaNatsume
en-aut-sei=Tada
en-aut-mei=Natsume
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=GotohAkira
en-aut-sei=Gotoh
en-aut-mei=Akira
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MagariMasaki
en-aut-sei=Magari
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HatanoNaoya
en-aut-sei=Hatano
en-aut-mei=Naoya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MorishitaRyo
en-aut-sei=Morishita
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=SunatsukiYukinari
en-aut-sei=Sunatsuki
en-aut-mei=Yukinari
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=NilssonUlf J.
en-aut-sei=Nilsson
en-aut-mei=Ulf J.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=IshikawaTeruhiko
en-aut-sei=Ishikawa
en-aut-mei=Teruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=TokumitsuHiroshi
en-aut-sei=Tokumitsu
en-aut-mei=Hiroshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

affil-num=1
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=6
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=8
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=9
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=10
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=CellFree Sciences Co. Ltd
kn-affil=

affil-num=12
en-affil=Organelle Systems Biotechnology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=13
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=14
en-affil=Department of Chemistry, Lund University
kn-affil=

affil-num=15
en-affil=Department of Science Education, Graduate School of Education, Okayama University
kn-affil=

affil-num=16
en-affil=Applied Cell Biology, Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=154
cd-vols=
no-issue=3
article-no=
start-page=209
end-page=217
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Attenuation of protein arginine dimethylation via S-nitrosylation of protein arginine methyltransferase 1
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Upregulation of nitric oxide (NO) production contributes to the pathogenesis of numerous diseases via S-nitro- sylation, a post-translational modification of proteins. This process occurs due to the oxidative reaction between NO and a cysteine thiol group; however, the extent of this reaction remains unknown. S-Nitrosylation of PRMT1, a major asymmetric arginine methyltransferase of histones and numerous RNA metabolic proteins, was induced by NO donor treatment. We found that nitrosative stress leads to S-nitrosylation of cysteine 119, located near the active site, and attenuates the enzymatic activity of PRMT1. Interestingly, RNA sequencing analysis revealed similarities in the changes in expression elicited by NO and PRMT1 inhibitors or knockdown. A comprehensive search for PRMT1 substrates using the proximity-dependent biotin identification method highlighted many known and new substrates, including RNA-metabolizing enzymes. To validate this result, we selected the RNA helicase DDX3 and demonstrated that arginine methylation of DDX3 is induced by PRMT1 and attenuated by NO treatment. Our results suggest the existence of a novel regulatory system associated with transcription and RNA metabolism via protein S-nitrosylation.
en-copyright=
kn-copyright=

en-aut-name=TaniguchiRikako
en-aut-sei=Taniguchi
en-aut-mei=Rikako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriyaYuto
en-aut-sei=Moriya
en-aut-mei=Yuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=DohmaeNaoshi
en-aut-sei=Dohmae
en-aut-mei=Naoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuzukiTakehiro
en-aut-sei=Suzuki
en-aut-mei=Takehiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakaharaKengo
en-aut-sei=Nakahara
en-aut-mei=Kengo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KubotaSho
en-aut-sei=Kubota
en-aut-mei=Sho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=

affil-num=3
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=4
en-affil=Biomolecular Characterization Unit, Technology Platform Division, RIKEN Center for Sustainable Resource Science
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University 
kn-affil=

affil-num=6
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Nitric oxide
kn-keyword=Nitric oxide
en-keyword=S-Nitrosylation
kn-keyword=S-Nitrosylation
en-keyword=Protein arginine methyltransferase 1 (PRMT1)
kn-keyword=Protein arginine methyltransferase 1 (PRMT1)
en-keyword=RNA metabolism
kn-keyword=RNA metabolism
en-keyword=Dead-box helicase 3X-linxed (DDX3)
kn-keyword=Dead-box helicase 3X-linxed (DDX3)
END

start-ver=1.4
cd-journal=joma
no-vol=65
cd-vols=
no-issue=3
article-no=
start-page=100510
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=202403
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Nuclear SphK2/S1P signaling is a key regulator of ApoE production and A�� uptake in astrocytes
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The link between changes in astrocyte function and the pathological progression of Alzheimer's disease (AD) has attracted considerable attention. Interestingly, activated astrocytes in AD show abnormalities in their lipid content and metabolism. In particular, the expression of apolipoprotein E (ApoE), a lipid transporter, is decreased. Because ApoE has anti-inflammatory and amyloid �� (A��)-metabolizing effects, the nuclear receptors, retinoid X receptor (RXR) and LXR, which are involved in ApoE expression, are considered promising therapeutic targets for AD. However, the therapeutic effects of agents targeting these receptors are limited or vary considerably among groups, indicating the involvement of an unknown pathological factor that modifies astrocyte and ApoE function. Here, we focused on the signaling lipid, sphingosine-1-phosphate (S1P), which is mainly produced by sphingosine kinase 2 (SphK2) in the brain. Using astrocyte models, we found that upregulation of SphK2/S1P signaling suppressed ApoE induction by both RXR and LXR agonists. We also found that SphK2 activation reduced RXR binding to the APOE promoter region in the nucleus, suggesting the nuclear function of SphK2/S1P. Intriguingly, suppression of SphK2 activity by RNA knockdown or specific inhibitors upregulated lipidated ApoE induction. Furthermore, the induced ApoE facilitates A�� uptake in astrocytes. Together with our previous findings that SphK2 activity is upregulated in AD brain and promotes A�� production in neurons, these results indicate that SphK2/S1P signaling is a promising multifunctional therapeutic target for AD that can modulate astrocyte function by stabilizing the effects of RXR and LXR agonists, and simultaneously regulate neuronal pathogenesis.
en-copyright=
kn-copyright=

en-aut-name=KomaiMasato
en-aut-sei=Komai
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NodaYuka
en-aut-sei=Noda
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IkedaAtsuya
en-aut-sei=Ikeda
en-aut-mei=Atsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KaneshiroNanaka
en-aut-sei=Kaneshiro
en-aut-mei=Nanaka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KamikuboYuji
en-aut-sei=Kamikubo
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SakuraiTakashi
en-aut-sei=Sakurai
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TakasugiNobumasa
en-aut-sei=Takasugi
en-aut-mei=Nobumasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=6
en-affil=Department of Cellular and Molecular Pharmacology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=alzheimer's disease
kn-keyword=alzheimer's disease
en-keyword=apolipoproteins
kn-keyword=apolipoproteins
en-keyword=nuclear receptors/RXR
kn-keyword=nuclear receptors/RXR
en-keyword=transcription
kn-keyword=transcription
en-keyword=sphingosine phosphate
kn-keyword=sphingosine phosphate
en-keyword=astrocytes
kn-keyword=astrocytes
en-keyword=amyloid ��
kn-keyword=amyloid ��
en-keyword=sphingosine kinase 2
kn-keyword=sphingosine kinase 2
en-keyword=low-density lipoprotein receptor-related protein 4
kn-keyword=low-density lipoprotein receptor-related protein 4
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=6
article-no=
start-page=3523
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240320
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Suppression of Borna Disease Virus Replication during Its Persistent Infection Using the CRISPR/Cas13b System
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Borna disease virus (BoDV-1) is a bornavirus that infects the central nervous systems of various animal species, including humans, and causes fatal encephalitis. BoDV-1 also establishes persistent infection in neuronal cells and causes neurobehavioral abnormalities. Once neuronal cells or normal neural networks are lost by BoDV-1 infection, it is difficult to regenerate damaged neural networks. Therefore, the development of efficient anti-BoDV-1 treatments is important to improve the outcomes of the infection. Recently, one of the clustered regularly interspaced short palindromic repeats (CRISPRs) and CRISPR-associated (Cas) systems, CRISPR/Cas13, has been utilized as antiviral tools. However, it is still unrevealed whether the CRISPR/Cas13 system can suppress RNA viruses in persistently infected cells. In this study, we addressed this question using persistently BoDV-1-infected cells. The CRISPR/Cas13 system targeting viral mRNAs efficiently decreased the levels of target viral mRNAs and genomic RNA (gRNA) in persistently infected cells. Furthermore, the CRISPR/Cas13 system targeting viral mRNAs also suppressed BoDV-1 infection if the system was introduced prior to the infection. Collectively, we demonstrated that the CRISPR/Cas13 system can suppress BoDV-1 in both acute and persistent infections. Our findings will open the avenue to treat prolonged infection with RNA viruses using the CRISPR/Cas13 system.
en-copyright=
kn-copyright=

en-aut-name=SasakiShigenori
en-aut-sei=Sasaki
en-aut-mei=Shigenori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OgawaHirohito
en-aut-sei=Ogawa
en-aut-mei=Hirohito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KatohHirokazu
en-aut-sei=Katoh
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HondaTomoyuki
en-aut-sei=Honda
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Virology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=antiviral
kn-keyword=antiviral
en-keyword=antivirals
kn-keyword=antivirals
en-keyword=Borna disease virus
kn-keyword=Borna disease virus
en-keyword=CRISPR/Cas13b
kn-keyword=CRISPR/Cas13b
en-keyword=persistent infection
kn-keyword=persistent infection
END

start-ver=1.4
cd-journal=joma
no-vol=130
cd-vols=
no-issue=9
article-no=
start-page=1493
end-page=1504
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PRRX1-TOP2A interaction is a malignancy-promoting factor in human malignant peripheral nerve sheath tumours
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Paired related-homeobox 1 (PRRX1) is a transcription factor in the regulation of developmental morphogenetic processes. There is growing evidence that PRRX1 is highly expressed in certain cancers and is critically involved in human survival prognosis. However, the molecular mechanism of PRRX1 in cancer malignancy remains to be elucidated.<br>
Methods: PRRX1 expression in human Malignant peripheral nerve sheath tumours (MPNSTs) samples was detected immunohistochemically to evaluate survival prognosis. MPNST models with PRRX1 gene knockdown or overexpression were constructed in vitro and the phenotype of MPNST cells was evaluated. Bioinformatics analysis combined with co-immunoprecipitation, mass spectrometry, RNA-seq and structural prediction were used to identify proteins interacting with PRRX1.<br>
Results: High expression of PRRX1 was associated with a poor prognosis for MPNST. PRRX1 knockdown suppressed the tumorigenic potential. PRRX1 overexpressed in MPNSTs directly interacts with topoisomerase 2?A (TOP2A) to cooperatively promote epithelial-mesenchymal transition and increase expression of tumour malignancy-related gene sets including mTORC1, KRAS and SRC signalling pathways. Etoposide, a TOP2A inhibitor used in the treatment of MPNST, may exhibit one of its anticancer effects by inhibiting the PRRX1?TOP2A interaction.<br>
Conclusion: Targeting the PRRX1?TOP2A interaction in malignant tumours with high PRRX1 expression might provide a novel tumour-selective therapeutic strategy.
en-copyright=
kn-copyright=

en-aut-name=TakihiraShota
en-aut-sei=Takihira
en-aut-mei=Shota
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamadaDaisuke
en-aut-sei=Yamada
en-aut-mei=Daisuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OsoneTatsunori
en-aut-sei=Osone
en-aut-mei=Tatsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TakaoTomoka
en-aut-sei=Takao
en-aut-mei=Tomoka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SakaguchiMasakiyo
en-aut-sei=Sakaguchi
en-aut-mei=Masakiyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HakozakiMichiyuki
en-aut-sei=Hakozaki
en-aut-mei=Michiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ItanoTakuto
en-aut-sei=Itano
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=KunisadaToshiyuki
en-aut-sei=Kunisada
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=TakaradaTakeshi
en-aut-sei=Takarada
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Orthopedic Surgery, Fukushima Medical University School of Medicine
kn-affil=

affil-num=7
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Orthopedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Regenerative Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=15
cd-vols=
no-issue=3
article-no=
start-page=153
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240309
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=A Survey of AI Techniques in IoT Applications with Use Case Investigations in the Smart Environmental Monitoring and Analytics in Real-Time IoT Platform
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In this paper, we have developed the SEMAR (Smart Environmental Monitoring and Analytics in Real-Time) IoT application server platform for fast deployments of IoT application systems. It provides various integration capabilities for the collection, display, and analysis of sensor data on a single platform. Recently, Artificial Intelligence (AI) has become very popular and widely used in various applications including IoT. To support this growth, the integration of AI into SEMAR is essential to enhance its capabilities after identifying the current trends of applicable AI technologies in IoT applications. In this paper, we first provide a comprehensive review of IoT applications using AI techniques in the literature. They cover predictive analytics, image classification, object detection, text spotting, auditory perception, Natural Language Processing (NLP), and collaborative AI. Next, we identify the characteristics of each technique by considering the key parameters, such as software requirements, input/output (I/O) data types, processing methods, and computations. Third, we design the integration of AI techniques into SEMAR based on the findings. Finally, we discuss use cases of SEMAR for IoT applications with AI techniques. The implementation of the proposed design in SEMAR and its use to IoT applications will be in future works.
en-copyright=
kn-copyright=

en-aut-name=PandumanYohanes Yohanie Fridelin
en-aut-sei=Panduman
en-aut-mei=Yohanes Yohanie Fridelin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FunabikiNobuo
en-aut-sei=Funabiki
en-aut-mei=Nobuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FajriantiEvianita Dewi
en-aut-sei=Fajrianti
en-aut-mei=Evianita Dewi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=FangShihao
en-aut-sei=Fang
en-aut-mei=Shihao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=SukaridhotoSritrusta
en-aut-sei=Sukaridhoto
en-aut-mei=Sritrusta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Natural Science and Technology, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Informatic and Computer, Politeknik Elektronika Negeri Surabaya
kn-affil=
en-keyword=Internet of Things
kn-keyword=Internet of Things
en-keyword=AI
kn-keyword=AI
en-keyword=integration
kn-keyword=integration
en-keyword=survey
kn-keyword=survey
en-keyword=application server platform
kn-keyword=application server platform
en-keyword=SEMAR
kn-keyword=SEMAR
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=
article-no=
start-page=28201
end-page=28211
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=WLAN Channel Status Duration Prediction for Audio and Video Services Using Probabilistic Neural Networks
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Due to massive increase in wireless access from smartphones, IoT devices, WLAN is aiming to improve its spectrum efficiency (SE) using many technologies. Some interesting techniques for WLAN systems are flexible allocation of frequency resource and cognitive radio (CR) techniques which expect to find more useful spectrum resource by modeling and then predicting of channel status using the captured statistics information of the used spectrum. This paper investigates the prediction accuracy of busy/idle duration of two major wireless services: audio service and video service using neural network based predictor. We first study the statistics distribution of their time-series busy/idle (B/I) duration, and then analyze the predictability of the busy/idle duration based on the predictability theory. Then, we propose a data categorization (DC) method which categorizes the duration of recent B/I duration according the their ranges to make the duration of next data be distributed into several streams. From the predictability analysis of each stream and the prediction performance using the probabilistic neural network (PNN), it can be confirmed that the proposed DC can improve the prediction accuracy of time-series data in partial streams.
en-copyright=
kn-copyright=

en-aut-name=HouYafei
en-aut-sei=Hou
en-aut-mei=Yafei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=DennoSatoshi
en-aut-sei=Denno
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=

affil-num=2
en-affil=Faculty of Environmental, Life, Natural Science and Technology, Okayama University
kn-affil=
en-keyword=Wireless LAN
kn-keyword=Wireless LAN
en-keyword=Wireless communication
kn-keyword=Wireless communication
en-keyword=Media streaming
kn-keyword=Media streaming
en-keyword=Wireless sensor networks
kn-keyword=Wireless sensor networks
en-keyword=Resource management
kn-keyword=Resource management
en-keyword=Probability distribution
kn-keyword=Probability distribution
en-keyword=Channel allocation
kn-keyword=Channel allocation
en-keyword=Audio-visual systems
kn-keyword=Audio-visual systems
en-keyword=Data processing
kn-keyword=Data processing
en-keyword=Predictive models
kn-keyword=Predictive models
en-keyword=Neural networks
kn-keyword=Neural networks
en-keyword=Channel status duration prediction
kn-keyword=Channel status duration prediction
en-keyword=WLAN audio/video traffic
kn-keyword=WLAN audio/video traffic
en-keyword=data predictability analysis
kn-keyword=data predictability analysis
en-keyword=probabilistic neural network (PNN)
kn-keyword=probabilistic neural network (PNN)
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=3
article-no=
start-page=889
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240203
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Characteristics of Functional Hyperthermia Detected in an Outpatient Clinic for Fever of Unknown Origin
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background: Functional hyperthermia (FH) is characterized by hyperthermia resulting from sympathetic hyperactivity rather than inflammation, and it is frequently overlooked by medical practitioners due to the absence of abnormalities in a medical examination. Although FH is an important differential diagnosis for fever of unknown origin (FUO), the literature on FUO cases in Japan lacks information on FH. In this study, we aimed to uncover the population of FH patients hidden in FUO cases. Methods: An outpatient clinic for FUO was established at Okayama University Hospital, and 132 patients were examined during the period from May 2019 to February 2022. Results: A diagnosis of FH was made in 31.1% of the FUO cases, and FH predominantly affected individuals in their third and fourth decades of life with a higher incidence in females (68.3%). The frequency of a history of psychiatric illness was higher in patients with FH than in patients with other febrile illnesses. Although the C-reactive protein (CRP) is generally negative in FH cases, some obese patients, with a body mass index >= 25 had slightly elevated levels of CRP but were diagnosed with FH. Conclusions: The results showed the importance of identifying FH when encountering patients with FUO without any organic etiology.
en-copyright=
kn-copyright=

en-aut-name=OkaKosuke
en-aut-sei=Oka
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=C-reactive protein (CRP)
kn-keyword=C-reactive protein (CRP)
en-keyword=fever of unknown origin (FUO)
kn-keyword=fever of unknown origin (FUO)
en-keyword=functional hyperthermia (FH)
kn-keyword=functional hyperthermia (FH)
en-keyword=psychiatric disorder
kn-keyword=psychiatric disorder
en-keyword=psychogenic fever
kn-keyword=psychogenic fever
END

start-ver=1.4
cd-journal=joma
no-vol=299
cd-vols=
no-issue=8
article-no=
start-page=105020
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202308
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mammalian type opsin 5 preferentially activates G14 in Gq-type G proteins triggering intracellular calcium response
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Mammalian type opsin 5 (Opn5m), a UV-sensitive G protein-coupled receptor opsin highly conserved in vertebrates, would provide a common basis for UV sensing from lamprey to humans. However, G protein coupled with Opn5m remains controversial due to variations in assay conditions and the origin of Opn5m across different reports. Here, we examined Opn5m from diverse species using an aequorin luminescence assay and G alpha-KO cell line. Beyond the commonly studied major G alpha classes, G alpha q, G alpha 11, G alpha 14, and G alpha 15 in the Gq class were individually investigated in this study, as they can drive distinct signaling pathways in addition to a canonical calcium response. UV light triggered a calcium response via all the tested Opn5m proteins in 293T cells, which was abolished by Gq-type G alpha deletion and rescued by cotransfection with mouse and medaka Gq-type G alpha proteins. Opn5m preferentially activated G alpha 14 and close relatives. Mutational analysis implicated specific regions, including alpha 3-beta 5 and alpha G-alpha 4 loops, alpha G and alpha 4 helices, and the extreme C terminus, in the preferential activation of G alpha 14 by Opn5m. FISH revealed co-expression of genes encoding Opn5m and G alpha 14 in the scleral cartilage of medaka and chicken eyes, supporting their physiological coupling. This suggests that the preferential activation of G alpha 14 by Opn5m is relevant for UV sensing in specific cell types.
en-copyright=
kn-copyright=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YamashitaTakahiro
en-aut-sei=Yamashita
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Biophysics, Graduate School of Science, Kyoto University
kn-affil=

affil-num=3
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=G protein
kn-keyword=G protein
en-keyword=G protein?coupled receptor (GPCR)
kn-keyword=G protein?coupled receptor (GPCR)
en-keyword=photoreceptor
kn-keyword=photoreceptor
en-keyword=rhodopsin
kn-keyword=rhodopsin
en-keyword=calcium intracellular release
kn-keyword=calcium intracellular release
en-keyword=protein?protein interaction
kn-keyword=protein?protein interaction
en-keyword=signal transduction
kn-keyword=signal transduction
en-keyword=nonvisual photoreception
kn-keyword=nonvisual photoreception
END

start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=e0296408
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240105
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Aromatic oil from lavender as an atopic dermatitis suppressant
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.
en-copyright=
kn-copyright=

en-aut-name=SatoHaruna
en-aut-sei=Sato
en-aut-mei=Haruna
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=KatoKosuke
en-aut-sei=Kato
en-aut-mei=Kosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KoreishiMayuko
en-aut-sei=Koreishi
en-aut-mei=Mayuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=NakamuraYoshimasa
en-aut-sei=Nakamura
en-aut-mei=Yoshimasa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsujinoYoshio
en-aut-sei=Tsujino
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SatohAyano
en-aut-sei=Satoh
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Science, Technology, and Innovation, Kobe University
kn-affil=

affil-num=6
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=49
cd-vols=
no-issue=2
article-no=
start-page=55
end-page=60
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=2024
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Methylmercury-induced brain neuronal death in CHOP-knockout mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Apoptosis is one of the hallmarks of MeHg-induced neuronal cell death; however, its molecular mechanism remains unclear. We previously reported that MeHg exposure induces neuron-specific ER stress in the mouse brain. Excessive ER stress contributes to apoptosis, and CHOP induction is considered to be one of the major mechanisms. CHOP is also increased by MeHg exposure in the mouse brain, suggesting that it correlates with increased apoptosis. In this study, to clarify whether CHOP mediates MeHg-induced apoptosis, we examined the effect of CHOP deletion on MeHg exposure in CHOP-knockout mice. Our data showed that CHOP deletion had no effect on MeHg exposure-induced weight loss or hindlimb impairment in mice, nor did it increase apoptosis or inhibit neuronal cell loss. Hence, CHOP plays little role in MeHg toxicity, and other apoptotic pathways coupled with ER stress may be involved in MeHg-induced cell death.
en-copyright=
kn-copyright=

en-aut-name=IijimaYuta
en-aut-sei=Iijima
en-aut-mei=Yuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MikiRyohei
en-aut-sei=Miki
en-aut-mei=Ryohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=FujimuraMasatake
en-aut-sei=Fujimura
en-aut-mei=Masatake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OyadomariSeiichi
en-aut-sei=Oyadomari
en-aut-mei=Seiichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=UeharaTakashi
en-aut-sei=Uehara
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Basic Medical Science, National Institute for Minamata Disease
kn-affil=

affil-num=4
en-affil=Division of Molecular Biology, Institute of Advanced Medical Sciences, Tokushima University
kn-affil=

affil-num=5
en-affil=Department of Medicinal Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Methylmercury
kn-keyword=Methylmercury
en-keyword=Neuronal cell death
kn-keyword=Neuronal cell death
en-keyword=Apoptosis
kn-keyword=Apoptosis
en-keyword=CHOP
kn-keyword=CHOP
en-keyword=Knockout mouse
kn-keyword=Knockout mouse
END

start-ver=1.4
cd-journal=joma
no-vol=25
cd-vols=
no-issue=3
article-no=
start-page=1585
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240127
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Mutual Effects of Orexin and Bone Morphogenetic Proteins on Catecholamine Regulation Using Adrenomedullary Cells
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Orexins are neuronal peptides that play a prominent role in sleep behavior and feeding behavior in the central nervous system, though their receptors also exist in peripheral organs, including the adrenal gland. In this study, the effects of orexins on catecholamine synthesis in the rat adrenomedullary cell line PC12 were investigated by focusing on their interaction with the adrenomedullary bone morphogenetic protein (BMP)-4. Orexin A treatment reduced the mRNA levels of key enzymes for catecholamine synthesis, including tyrosine hydroxylase (Th), 3,4-dihydroxyphenylalanie decarboxylase (Ddc) and dopamine beta-hydroxylase (Dbh), in a concentration-dependent manner. On the other hand, treatment with BMP-4 suppressed the expression of Th and Ddc but enhanced that of Dbh with or without co-treatment with orexin A. Of note, orexin A augmented BMP-receptor signaling detected by the phosphorylation of Smad1/5/9 through the suppression of inhibitory Smad6/7 and the upregulation of BMP type-II receptor (BMPRII). Furthermore, treatment with BMP-4 upregulated the mRNA levels of OX1R in PC12 cells. Collectively, the results indicate that orexin and BMP-4 suppress adrenomedullary catecholamine synthesis by mutually upregulating the pathway of each other in adrenomedullary cells.
en-copyright=
kn-copyright=

en-aut-name=SoejimaYoshiaki
en-aut-sei=Soejima
en-aut-mei=Yoshiaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IwataNahoko
en-aut-sei=Iwata
en-aut-mei=Nahoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SuyamaAtsuhito
en-aut-sei=Suyama
en-aut-mei=Atsuhito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=bone morphogenetic protein (BMP)
kn-keyword=bone morphogenetic protein (BMP)
en-keyword=orexin
kn-keyword=orexin
en-keyword=catecholamine and adrenal
kn-keyword=catecholamine and adrenal
END

start-ver=1.4
cd-journal=joma
no-vol=115
cd-vols=
no-issue=3
article-no=
start-page=871
end-page=882
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240126
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Role of catecholamine synthases in the maintenance of cancer stem-like cells in malignant peripheral nerve sheath tumors
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Malignant peripheral nerve sheath tumors (MPNSTs) are malignant tumors that are derived from Schwann cell lineage around peripheral nerves. As in many other cancer types, cancer stem cells (CSCs) have been identified in MPNSTs, and they are considered the cause of treatment resistance, recurrence, and metastasis. As an element defining the cancer stemness of MPNSTs, we previously reported a molecular mechanism by which exogenous adrenaline activates a core cancer stemness factor, YAP/TAZ, through ��2 adrenoceptor (ADRB2). In this study, we found that MPNST cells express catecholamine synthases and that these enzymes are essential for maintaining cancer stemness, such as the ability to self-renew and maintain an undifferentiated state. Through gene knockdown and inhibition of these enzymes, we confirmed that catecholamines are indeed synthesized in MPNST cells. The results confirmed that catecholamine synthase knockdown in MPNST cells reduces the activity of YAP/TAZ. These data suggest that a mechanism of YAP/TAZ activation by de novo synthesized adrenaline, as well as exogenous adrenaline, may exist in the maintenance of cancer stemness of MPNST cells. This mechanism not only helps to understand the pathology of MPNST, but could also contribute to the development of therapeutic strategies for MPNST.
en-copyright=
kn-copyright=

en-aut-name=KatayamaHaruyoshi
en-aut-sei=Katayama
en-aut-mei=Haruyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=FujimuraAtsushi
en-aut-sei=Fujimura
en-aut-mei=Atsushi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HuangRongsheng
en-aut-sei=Huang
en-aut-mei=Rongsheng
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=OtaniYusuke
en-aut-sei=Otani
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItanoTakuto
en-aut-sei=Itano
en-aut-mei=Takuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=FujiwaraTomohiro
en-aut-sei=Fujiwara
en-aut-mei=Tomohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KunisadaToshiyuki
en-aut-sei=Kunisada
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NakataEiji
en-aut-sei=Nakata
en-aut-mei=Eiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=OzakiToshifumi
en-aut-sei=Ozaki
en-aut-mei=Toshifumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=2
en-affil=Department of Cellular Physiology,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=3
en-affil=Department of Trauma Orthopedics,  The Second Hospital of Dalian Medical  University
kn-affil=

affil-num=4
en-affil=Department of General Thoracic Surgery  and Breast and Endocrinological Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=5
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=6
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=7
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=8
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=

affil-num=9
en-affil=Department of Orthopedic Surgery,  Okayama University Graduate School of  Medicine, Dentistry, and Pharmaceutical  Sciences
kn-affil=
en-keyword=benserazide
kn-keyword=benserazide
en-keyword=cancer stem cell
kn-keyword=cancer stem cell
en-keyword=catecholamine synthase
kn-keyword=catecholamine synthase
en-keyword=malignant peripheral nerve sheath tumor
kn-keyword=malignant peripheral nerve sheath tumor
en-keyword=Schwann cell
kn-keyword=Schwann cell
en-keyword=vesicular monoamine transporter
kn-keyword=vesicular monoamine transporter
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=2
article-no=
start-page=370
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Morphometric Analysis of the Eye by Magnetic Resonance Imaging in MGST2-Gene-Deficient Mice
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Strabismus, a neuro-ophthalmological condition characterized by misalignment of the eyes, is a common ophthalmic disorder affecting both children and adults. In our previous study, we identified the microsomal glutathione S-transferase 2 (MGST2) gene as one of the potential candidates for comitant strabismus susceptibility in a Japanese population. The MGST2 gene belongs to the membrane-associated protein involved in the generation of pro-inflammatory mediators, and it is also found in the protection against oxidative stress by decreasing the reactivity of oxidized lipids. To look for the roles of the MGST2 gene in the development, eye alignment, and overall morphology of the eye as the possible background of strabismus, MGST2 gene knockout (KO) mice were generated by CRISPR/Cas9-mediated gene editing with guide RNAs targeting the MGST2 exon 2. The ocular morphology of the KO mice was analyzed through high-resolution images obtained by a magnetic resonance imaging (MRI) machine for small animals. The morphometric analyses showed that the height, width, and volume of the eyeballs in MGST2 KO homozygous mice were significantly greater than those of wild-type mice, indicating that the eyes of MGST2 KO homozygous mice were significantly enlarged. There were no significant differences in the axis length and axis angle. These morphological changes may potentially contribute to the development of a subgroup of strabismus.
en-copyright=
kn-copyright=

en-aut-name=Chaomulige
en-aut-sei=Chaomulige
en-aut-mei=
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsuoToshihiko
en-aut-sei=Matsuo
en-aut-mei=Toshihiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SugimotoKohei
en-aut-sei=Sugimoto
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=MiyajiMary
en-aut-sei=Miyaji
en-aut-mei=Mary
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HosoyaOsamu
en-aut-sei=Hosoya
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=UedaMasashi
en-aut-sei=Ueda
en-aut-mei=Masashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KobayashiRyosuke
en-aut-sei=Kobayashi
en-aut-mei=Ryosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HoriiTakuro
en-aut-sei=Horii
en-aut-mei=Takuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=HatadaIzuho
en-aut-sei=Hatada
en-aut-mei=Izuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil= Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Medical Neurobiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Medical Neurobiology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Biofunctional Imaging Analysis, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=8
en-affil=Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=

affil-num=9
en-affil=Biosignal Genome Resource Center, Institute for Molecular and Cellular Regulation, Gunma University
kn-affil=
en-keyword=comitant strabismus
kn-keyword=comitant strabismus
en-keyword=MGST2 gene
kn-keyword=MGST2 gene
en-keyword=mouse models
kn-keyword=mouse models
en-keyword=genetics
kn-keyword=genetics
en-keyword=CRISPR/Cas9
kn-keyword=CRISPR/Cas9
en-keyword=PCR
kn-keyword=PCR
en-keyword=MRI
kn-keyword=MRI
en-keyword=eye morphology
kn-keyword=eye morphology
en-keyword=neuro-ophthalmology
kn-keyword=neuro-ophthalmology
END

start-ver=1.4
cd-journal=joma
no-vol=45
cd-vols=
no-issue=1
article-no=
start-page=2305899
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240125
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Clinical characteristics of female long COVID patients with menstrual symptoms: a retrospective study from a Japanese outpatient clinic
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: To elucidate the impact of long COVID on menstruation and mental health, medical records of patients with long COVID were evaluated.<br>
Methods: Symptoms of long COVID, QOL, mental health, and related endocrine data were compared between two groups with and without menstrual disturbances.<br>
Results: Of 349 female patients who visited our clinic between February 2021 and March 2023, 223 patients with long COVID (aged 18-50 years) were included. Forty-four (19.7%) of the patients had menstrual symptoms associated with long COVID. The patients with menstrual symptoms were older than those without menstrual symptoms (42.5 vs. 38 years). The percentage of patients with menstrual symptoms was higher during the Omicron phase (24%) than during the Preceding (13%) and Delta (12%) phases. Cycle irregularity was the most frequent (in 63.6% of the patients), followed by severe pain (25%), heavy bleeding (20.5%), perimenopausal symptoms (18.2%), and premenstrual syndrome (15.9%). Fatigue and depression were the most frequent complications. Scores for fatigue and for QOL were significantly worse in long COVID patients with menstrual symptoms. Results of endocrine examinations showed significantly increased cortisol levels in patients with menstrual complaints.<br>
Conclusion: Long COVID has an impact on menstrual conditions and on QOL related to menstrual conditions.
en-copyright=
kn-copyright=

en-aut-name=SakuradaYasue
en-aut-sei=Sakurada
en-aut-mei=Yasue
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatsudaYui
en-aut-sei=Matsuda
en-aut-mei=Yui
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MotohashiKanon
en-aut-sei=Motohashi
en-aut-mei=Kanon
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HasegawaToru
en-aut-sei=Hasegawa
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OtsukaYuki
en-aut-sei=Otsuka
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=NakanoYasuhiro
en-aut-sei=Nakano
en-aut-mei=Yasuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TokumasuKazuki
en-aut-sei=Tokumasu
en-aut-mei=Kazuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=YamamotoKoichiro
en-aut-sei=Yamamoto
en-aut-mei=Koichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SunadaNaruhiko
en-aut-sei=Sunada
en-aut-mei=Naruhiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=HondaHiroyuki
en-aut-sei=Honda
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HagiyaHideharu
en-aut-sei=Hagiya
en-aut-mei=Hideharu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=UedaKeigo
en-aut-sei=Ueda
en-aut-mei=Keigo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=OtsukaFumio
en-aut-sei=Otsuka
en-aut-mei=Fumio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

affil-num=1
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Infectious Diseases, Okayama University Hospital
kn-affil=

affil-num=12
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=13
en-affil=Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Depression
kn-keyword=Depression
en-keyword=fatigue
kn-keyword=fatigue
en-keyword=menstrual symptoms
kn-keyword=menstrual symptoms
en-keyword=omicron variant
kn-keyword=omicron variant
en-keyword=post-COVID-19 condition
kn-keyword=post-COVID-19 condition
END

start-ver=1.4
cd-journal=joma
no-vol=12
cd-vols=
no-issue=1
article-no=
start-page=118
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240106
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Hydrogen in Transplantation: Potential Applications and Therapeutic Implications
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hydrogen gas, renowned for its antioxidant properties, has emerged as a novel therapeutic agent with applications across various medical domains, positioning it as a potential adjunct therapy in transplantation. Beyond its antioxidative properties, hydrogen also exerts anti-inflammatory effects by modulating pro-inflammatory cytokines and signaling pathways. Furthermore, hydrogen's capacity to activate cytoprotective pathways bolsters cellular resilience against stressors. In recent decades, significant advancements have been made in the critical medical procedure of transplantation. However, persistent challenges such as ischemia-reperfusion injury (IRI) and graft rejection continue to hinder transplant success rates. This comprehensive review explores the potential applications and therapeutic implications of hydrogen in transplantation, shedding light on its role in mitigating IRI, improving graft survival, and modulating immune responses. Through a meticulous analysis encompassing both preclinical and clinical studies, we aim to provide valuable insights into the promising utility of hydrogen as a complementary therapy in transplantation.
en-copyright=
kn-copyright=

en-aut-name=ObaraTakafumi
en-aut-sei=Obara
en-aut-mei=Takafumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NaitoHiromichi
en-aut-sei=Naito
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NojimaTsuyoshi
en-aut-sei=Nojima
en-aut-mei=Tsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HirayamaTakahiro
en-aut-sei=Hirayama
en-aut-mei=Takahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=HongoTakashi
en-aut-sei=Hongo
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=AgetaKohei
en-aut-sei=Ageta
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=AokageToshiyuki
en-aut-sei=Aokage
en-aut-mei=Toshiyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=HisamuraMasaki
en-aut-sei=Hisamura
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YumotoTetsuya
en-aut-sei=Yumoto
en-aut-mei=Tetsuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NakaoAtsunori
en-aut-sei=Nakao
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Emergency, Critical Care, and Disaster Medicine, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=hydrogen
kn-keyword=hydrogen
en-keyword=organ transplantation
kn-keyword=organ transplantation
en-keyword=ischemia reperfusion
kn-keyword=ischemia reperfusion
END

start-ver=1.4
cd-journal=joma
no-vol=24
cd-vols=
no-issue=18
article-no=
start-page=14128
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230915
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Advanced Techniques Using In Vivo Electroporation to Study the Molecular Mechanisms of Cerebral Development Disorders
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The mammalian cerebral cortex undergoes a strictly regulated developmental process. Detailed in situ visualizations, imaging of these dynamic processes, and in vivo functional gene studies significantly enhance our understanding of brain development and related disorders. This review introduces basic techniques and recent advancements in in vivo electroporation for investigating the molecular mechanisms underlying cerebral diseases. In utero electroporation (IUE) is extensively used to visualize and modify these processes, including the forced expression of pathological mutants in human diseases; thus, this method can be used to establish animal disease models. The advent of advanced techniques, such as genome editing, including de novo knockout, knock-in, epigenetic editing, and spatiotemporal gene regulation, has further expanded our list of investigative tools. These tools include the iON expression switch for the precise control of timing and copy numbers of exogenous genes and TEMPO for investigating the temporal effects of genes. We also introduce the iGONAD method, an improved genome editing via oviductal nucleic acid delivery approach, as a novel genome-editing technique that has accelerated brain development exploration. These advanced in vivo electroporation methods are expected to provide valuable insights into pathological conditions associated with human brain disorders.
en-copyright=
kn-copyright=

en-aut-name=YangChen
en-aut-sei=Yang
en-aut-mei=Chen
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShitamukaiAtsunori
en-aut-sei=Shitamukai
en-aut-mei=Atsunori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YangShucai
en-aut-sei=Yang
en-aut-mei=Shucai
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawaguchiAyano
en-aut-sei=Kawaguchi
en-aut-mei=Ayano
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Human Anatomy and Histology and Embryology, School of Basic Medicine, Harbin Medical University
kn-affil=

affil-num=4
en-affil=Department of Human Morphology, Okayama University Graduate School of Medicine, Density and Pharmaceutical Sciences
kn-affil=
en-keyword=in vivo electroporation
kn-keyword=in vivo electroporation
en-keyword=in utero electroporation
kn-keyword=in utero electroporation
en-keyword=genome editing
kn-keyword=genome editing
en-keyword=IUE
kn-keyword=IUE
en-keyword=iON
kn-keyword=iON
en-keyword=TEMPO
kn-keyword=TEMPO
en-keyword=iGONAD
kn-keyword=iGONAD
END

start-ver=1.4
cd-journal=joma
no-vol=113
cd-vols=
no-issue=
article-no=
start-page=61
end-page=73
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The List of Published by Members of the Faculty From January to December 2023.
kn-title=���\�w�p�_�������X�g�@2023
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=
END

start-ver=1.4
cd-journal=joma
no-vol=436
cd-vols=
no-issue=5
article-no=
start-page=168319
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2024
dt-pub=20240301
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Molecular Property, Manipulation, and Potential Use of Opn5 and Its Homologs
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Animal opsin is a G-protein coupled receptor (GPCR) and binds retinal as a chromophore to form a photopigment. The Opsin 5 (Opn5) group within the animal opsin family comprises a diverse array of related proteins, such as Opn5m, a protein conserved across all vertebrate lineages including mammals, and other members like Opn5L1 and Opn5L2 found in non-mammalian vertebrate genomes, and Opn6 found in non-therian vertebrate genomes, along with Opn5 homologs present in invertebrates. Although these proteins collectively constitute a single clade within the molecular phylogenetic tree of animal opsins, they exhibit markedly distinct molecular characteristics in areas such as retinal binding properties, photoreaction, and G-protein coupling specificity. Based on their molecular features, they are believed to play a significant role in physiological functions. However, our understanding of their precise physiological functions and molecular characteristics is still developing and only partially realized. Furthermore, their unique molecular characteristics of Opn5-related proteins suggest a high potential for their use as optogenetic tools through more specialized manipulations. This review intends to encapsulate our current understanding of Opn5, discuss potential manipulations of its molecular attributes, and delve into its prospective utility in the burgeoning field of animal opsin optogenetics.
en-copyright=
kn-copyright=

en-aut-name=SatoKeita
en-aut-sei=Sato
en-aut-mei=Keita
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhuchiHideyo
en-aut-sei=Ohuchi
en-aut-mei=Hideyo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Cytology and Histology, Faculty of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Opn5
kn-keyword=Opn5
en-keyword=rhodopsin
kn-keyword=rhodopsin
en-keyword=optogenetics
kn-keyword=optogenetics
en-keyword=retinal protein
kn-keyword=retinal protein
en-keyword=non-image-forming opsin
kn-keyword=non-image-forming opsin
END

start-ver=1.4
cd-journal=joma
no-vol=3
cd-vols=
no-issue=3
article-no=
start-page=100312
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=202309
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Epiretinal Membrane Impairs the Inner Retinal Layer in a Traction Force-Dependent Manner
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Purpose: To investigate the relationship between retinal traction force and impairment of the inner retinal layer in patients with epiretinal membrane (ERM).<br>
Design: Nonrandomized, retrospective consecutive case series.<br>
Participants: Two hundred nine eyes of 201 patients with idiopathic ERM who underwent vitrectomy for idiopathic ERM were enrolled.<br>
Methods: Retinal folds caused by ERM were visualized using en face OCT, and the maximum depth of retinal folds within the parafovea (MDRF) was measured. Focal macular electroretinogram (ERG) was used to measure the amplitude and implicit time of each component for the ERM eyes and the normal fellow eyes. B-scan OCT images were used to measure the thicknesses of the inner nuclear layer (INL) and outer nuclear layer (ONL) + outer plexiform layer (OPL). Expression of ��-smooth muscle actin (��-SMA) in surgically removed ERM specimens was quantified by reverse-transcription polymerase chain reaction.<br>
Main Outcome Measures: We analyzed the relationship between MDRF and the relative amplitudes of focal macular ERG (affected eye/fellow eye), the relationships between MDRF and the mean INL thickness and ONL+OPL thickness, comparison of INL thickness and ONL+OPL thickness for each area when cases were classified according to MDRF localization in the ETDRS chart, and the relationship between MDRF and the relative expression of ��-SMA in the ERM specimens.<br>
Results: The MDRF significantly correlated with the relative amplitudes (affected eye/fellow eye) of b-waves and oscillatory potentials (r = ?0.657, P = 0.015; r = ?0.569, P = 0.042, respectively) and the mean INL thickness and ONL+OPL thickness (r = 0.604, P < 0.001; r = 0.210, P = 0.007, respectively). However, only the INL thickness progression rate was significantly correlated with the MDRF progression rate (r = 0.770, P < 0.001). On case stratification by localization of MDRF based on the ETDRS chart, in regions other than temporal regions, the INL thickness was significantly greater in regions with MDRF than in other regions. The MDRF significantly correlated with ��-SMA expression in the ERM specimens (r = 0.555, P = 0.009).<br>
Conclusions: The findings suggest that ERM impairs the inner retinal layer in a traction force-dependent manner.<br>
Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

en-copyright=
kn-copyright=

en-aut-name=KanzakiYuki
en-aut-sei=Kanzaki
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MatobaRyo
en-aut-sei=Matoba
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KimuraShuhei
en-aut-sei=Kimura
en-aut-mei=Shuhei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=HosokawaMio M.
en-aut-sei=Hosokawa
en-aut-mei=Mio M.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ShiodeYusuke
en-aut-sei=Shiode
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=DoiShinichiro
en-aut-sei=Doi
en-aut-mei=Shinichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=MoritaTetsuro
en-aut-sei=Morita
en-aut-mei=Tetsuro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KanzakiSayumi
en-aut-sei=Kanzaki
en-aut-mei=Sayumi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TakasuIppei
en-aut-sei=Takasu
en-aut-mei=Ippei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TanikawaAtsuhiro
en-aut-sei=Tanikawa
en-aut-mei=Atsuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MorizaneYuki
en-aut-sei=Morizane
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

affil-num=1
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Takasu Eye Clinic
kn-affil=

affil-num=10
en-affil=Department of Ophthalmology, Fujita Health University Bantane Hospital
kn-affil=

affil-num=11
en-affil=Department of Ophthalmology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Epiretinal membrane
kn-keyword=Epiretinal membrane
en-keyword=En face OCT
kn-keyword=En face OCT
en-keyword=Retinal traction force
kn-keyword=Retinal traction force
en-keyword=Inner nuclear layer
kn-keyword=Inner nuclear layer
en-keyword=Focal macular electroretinogram
kn-keyword=Focal macular electroretinogram
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=12
article-no=
start-page=1706
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231124
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Roles of Human Endogenous Retroviruses and Endogenous Virus-Like Elements in Cancer Development and Innate Immunity
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Human endogenous retroviruses (HERVs) are remnants of ancient retroviral infections in the host genome. Although mutations and silencing mechanisms impair their original role in viral replication, HERVs are believed to play roles in various biological processes. Long interspersed nuclear elements (LINEs) are non-LTR retrotransposons that have a lifecycle resembling that of retroviruses. Although LINE expression is typically silenced in somatic cells, it also contributes to various biological processes. The aberrant expression of HERVs and LINEs is closely associated with the development of cancer and/or immunological diseases, suggesting that they are integrated into various pathways related to the diseases. HERVs/LINEs control gene expression depending on the context as promoter/enhancer elements. Some RNAs and proteins derived from HERVs/LINEs have oncogenic potential, whereas others stimulate innate immunity. Non-retroviral endogenous viral elements (nrEVEs) are a novel type of virus-like element in the genome. nrEVEs may also be involved in host immunity. This article provides a current understanding of how these elements impact cellular physiology in cancer development and innate immunity, and provides perspectives for future studies.
en-copyright=
kn-copyright=

en-aut-name=KatohHirokazu
en-aut-sei=Katoh
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HondaTomoyuki
en-aut-sei=Honda
en-aut-mei=Tomoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

affil-num=1
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Virology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=HERVs
kn-keyword=HERVs
en-keyword=LINEs
kn-keyword=LINEs
en-keyword=cancer
kn-keyword=cancer
en-keyword=innate immunity
kn-keyword=innate immunity
en-keyword=promoter
kn-keyword=promoter
en-keyword=enhancer
kn-keyword=enhancer
en-keyword=interferon signaling
kn-keyword=interferon signaling
END

start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=2
article-no=
start-page=609
end-page=622
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Protective Effects of Rivaroxaban on White Matter Integrity and Remyelination in a Mouse Model of Alzheimer�fs Disease Combined with Cerebral Hypoperfusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background:Alzheimer�fs disease (AD) is characterized by cognitive dysfunction and memory loss that is accompanied by pathological changes to white matter. Some clinical and animal research revealed that AD combined with chronic cerebral hypoperfusion (CCH) exacerbates AD progression by inducing blood-brain barrier dysfunction and fibrinogen deposition. Rivaroxaban, an anticoagulant, has been shown to reduce the rates of dementia in atrial fibrillation patients, but its effects on white matter and the underlying mechanisms are unclear. <br>
Objective:The main purpose of this study was to explore the therapeutic effect of rivaroxaban on the white matter of AD+CCH mice. <br>
Methods:In this study, the therapeutic effects of rivaroxaban on white matter in a mouse AD+CCH model were investigated to explore the potential mechanisms involving fibrinogen deposition, inflammation, and oxidative stress on remyelination in white matter. <br>
Results:The results indicate that rivaroxaban significantly attenuated fibrinogen deposition, fibrinogen-related microglia activation, oxidative stress, and enhanced demyelination in AD+CCH mice, leading to improved white matter integrity, reduced axonal damage, and restored myelin loss.<br> Conclusions:These findings suggest that long-term administration of rivaroxaban might reduce the risk of dementia.
en-copyright=
kn-copyright=

en-aut-name=BianZhihong
en-aut-sei=Bian
en-aut-mei=Zhihong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HuXinran
en-aut-sei=Hu
en-aut-mei=Xinran
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=LiuXia
en-aut-sei=Liu
en-aut-mei=Xia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YuHaibo
en-aut-sei=Yu
en-aut-mei=Haibo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=BianYuting
en-aut-sei=Bian
en-aut-mei=Yuting
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SunHongming
en-aut-sei=Sun
en-aut-mei=Hongming
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FukuiYusuke
en-aut-sei=Fukui
en-aut-mei=Yusuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=IshiuraHiroyuki
en-aut-sei=Ishiura
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=2
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=3
en-affil=Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=5
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=6
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=7
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=8
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=9
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=10
en-affil=Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=
en-keyword=Alzheimer�fs disease
kn-keyword=Alzheimer�fs disease
en-keyword=cerebral amyloid angiopathy
kn-keyword=cerebral amyloid angiopathy
en-keyword=chronic cerebral hypoperfusion
kn-keyword=chronic cerebral hypoperfusion
en-keyword=rivaroxaban
kn-keyword=rivaroxaban
en-keyword=white matter
kn-keyword=white matter
END

start-ver=1.4
cd-journal=joma
no-vol=32
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=2023
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Safety and Clinical Effects of a Muse Cell-Based Product in Patients With Amyotrophic Lateral Sclerosis: Results of a Phase 2 Clinical Trial
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of motor neurons. Multilineage-differentiating stress-enduring (Muse) cells are unique endogenous stem cells that show therapeutic effects on motor function in ALS mouse models. We conducted a single-center open phase II clinical trial to evaluate the safety and clinical effects of repeated intravenous injections of an allogenic Muse cell-based product, CL2020, in patients with ALS. Five patients with ALS received CL2020 intravenously once a month for a total of six doses. The primary endpoints were safety and tolerability, and the secondary endpoint was the rate of change in the Revised Amyotrophic Lateral Sclerosis Functional Rating Scale (ALSFRS-R) score. In addition, serum tumor necrosis factor-�� (TNF-��), interleukin-6 (IL-6), sphingosine-1-phosphate (S1P), cerebrospinal fluid chitotriosidase-1 (CHIT-1), and neurofilament light chain (NfL) levels were evaluated. The CL2020 treatment was highly tolerated without serious side effects. The ALSFRS-R score change trended upward at 12 months post-CL2020 treatment compared with that at 3 months pre-administration, but the difference was not statistically significant. Among five patients diagnosed with ALS, three exhibited a decrease in the rate of ALSFRS-R score change, one demonstrated an increase, and another showed no change. In addition, the patients�f serum IL-6 and TNF-�� levels and cerebrospinal fluid CHIT-1 and NfL levels increased for up to 6 months post-treatment; however, their serum S1P levels continuously decreased over 12 months. These findings indicate a favorable safety profile of CL2020 therapy. In the near future, a double-blind study of a larger number of ALS patients should be conducted to confirm the efficacy of ALS treatment with CL2020.
en-copyright=
kn-copyright=

en-aut-name=YamashitaToru
en-aut-sei=Yamashita
en-aut-mei=Toru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakanoYumiko
en-aut-sei=Nakano
en-aut-mei=Yumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SasakiRyo
en-aut-sei=Sasaki
en-aut-mei=Ryo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TadokoroKoh
en-aut-sei=Tadokoro
en-aut-mei=Koh
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=OmoteYoshio
en-aut-sei=Omote
en-aut-mei=Yoshio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YunokiTaijun
en-aut-sei=Yunoki
en-aut-mei=Taijun
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=KawaharaYuko
en-aut-sei=Kawahara
en-aut-mei=Yuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=MatsumotoNamiko
en-aut-sei=Matsumoto
en-aut-mei=Namiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TairaYuki
en-aut-sei=Taira
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=MatsuokaChika
en-aut-sei=Matsuoka
en-aut-mei=Chika
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=MoriharaRyuta
en-aut-sei=Morihara
en-aut-mei=Ryuta
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=11
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=12
en-affil=Department of Neurology, Okayama University Graduate School of  Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=amyotrophic lateral sclerosis
kn-keyword=amyotrophic lateral sclerosis
en-keyword=clinical trial
kn-keyword=clinical trial
en-keyword=CL2020
kn-keyword=CL2020
en-keyword=multilineage-differentiating stress-enduring (Muse) cells
kn-keyword=multilineage-differentiating stress-enduring (Muse) cells
en-keyword=intravenous administration
kn-keyword=intravenous administration
END

start-ver=1.4
cd-journal=joma
no-vol=127
cd-vols=
no-issue=5
article-no=
start-page=1398
end-page=1406
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220509
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Tactile angle discriminability improvement: contributions of working memory training and continuous attended sensory input
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Perceptual learning is commonly assumed to enhance perception through continuous attended sensory input. However, learning is generalizable to performance in untrained stimuli and tasks. Although previous studies have observed a possible generalization effect across tasks as a result of working memory (WM) training, comparisons of the contributions of WM training and continuous attended sensory input to perceptual learning generalization are still rare. Therefore, we compared which factors contributed most to perceptual generalization and investigated which skills acquired during WM training led to tactile generalization across tasks. Here, a Braille-like dot pattern matching n-back WM task was used as the WM training task, with four workload levels (0, 1, 2, and 3-back levels). A tactile angle discrimination (TAD) task was used as a pre- and posttest to assess improvements in tactile perception. Between tests, four subject groups were randomly assigned to four different workload n-back tasks to consecutively complete three sessions of training. The results showed that tactile n-back WM training could enhance TAD performance, with the 3-back training group having the highest TAD threshold improvement rate. Furthermore, the rate of WM capacity improvement on the 3-back level across training sessions was correlated with the rate of TAD threshold improvement. These findings suggest that continuous attended sensory input and enhanced WM capacity can lead to improvements in TAD ability, and that greater improvements in WM capacity can predict greater improvements in TAD performance.<br>
NEW & NOTEWORTHY Perceptual learning is not always specific to the trained task and stimuli. We demonstrate that both continuous attended sensory input and improved WM capacity can be used to enhance tactile angle discrimination (TAD) ability. Moreover, WM capacity improvement is important in generalizing the training effect to the TAD ability. These findings contribute to understanding the mechanism of perceptual learning generalization across tasks.
en-copyright=
kn-copyright=

en-aut-name=WangWu
en-aut-sei=Wang
en-aut-mei=Wu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YangJiajia
en-aut-sei=Yang
en-aut-mei=Jiajia
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YuYinghua
en-aut-sei=Yu
en-aut-mei=Yinghua
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=LiHuazhi
en-aut-sei=Li
en-aut-mei=Huazhi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=LiuYulong
en-aut-sei=Liu
en-aut-mei=Yulong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=YuYiyang
en-aut-sei=Yu
en-aut-mei=Yiyang
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YuJiabin
en-aut-sei=Yu
en-aut-mei=Jiabin
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TangXiaoyu
en-aut-sei=Tang
en-aut-mei=Xiaoyu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=YangJingjing
en-aut-sei=Yang
en-aut-mei=Jingjing
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TakahashiSatoshi
en-aut-sei=Takahashi
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=EjimaYoshimichi
en-aut-sei=Ejima
en-aut-mei=Yoshimichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=WuJinglong
en-aut-sei=Wu
en-aut-mei=Jinglong
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

affil-num=1
en-affil=School of Psychological and Cognitive Sciences, Peking University
kn-affil=

affil-num=2
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=3
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=4
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=5
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=6
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=7
en-affil=College of Information Engineering, China Jiliang University
kn-affil=

affil-num=8
en-affil=School of Psychology, Liaoning Collaborative Innovation Center of Children and Adolescents Healthy Personality Assessment and Cultivation, Liaoning Normal University
kn-affil=

affil-num=9
en-affil=School of Computer Science and Technology, Changchun University of Science and Technology
kn-affil=

affil-num=10
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=11
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=

affil-num=12
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=
en-keyword=continuous attended sensory input
kn-keyword=continuous attended sensory input
en-keyword=perceptual learning
kn-keyword=perceptual learning
en-keyword=tactile angle discriminability
kn-keyword=tactile angle discriminability
en-keyword=tactile generalization
kn-keyword=tactile generalization
en-keyword=working memory training
kn-keyword=working memory training
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20230925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=��҂ƍ���҂ɂ����鎋���o�����ƃN���X���[�_���ȃ��[�L���O�������g���[�j���O�Ɋւ��錤��
kn-title=Study on audiovisual integration and cross-modal working memory training in young and older adults 
en-subtitle=
kn-subtitle=
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kn-abstract=
en-copyright=
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en-aut-name=GuoAo
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en-aut-mei=Ao
kn-aut-name=�s��
kn-aut-sei=�s
kn-aut-mei=��
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
kn-affil=���R��w��w�@�w���X�V�X�e�������Ȋw������
END

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en-aut-name=WEIXINGQIANG
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kn-aut-name=鰋���
kn-aut-sei=�
kn-aut-mei=����
aut-affil-num=1
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affil-num=1
en-affil=Graduate School of Environmental and Life Science, Okayama University
kn-affil=���R��w��w�@�������Ȋw������
END

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en-title=�}���`���f�B�A�R���e���c��ی삷�邽�߂̓d�q�������Ɋւ��錤��
kn-title=A Study of Digital Watermarking for Protecting the Multimedia Content
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en-aut-name=YASUITatsuya
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kn-aut-sei=����
kn-aut-mei=�B��
aut-affil-num=1
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affil-num=1
en-affil=Graduate School of Natural Science and Technology, Okayama university
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kn-title=Oxytocin enhances progesterone production with upregulation of BMP-15 activity by granulosa cells
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en-aut-name=YAMAMOTOKoichiro
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affil-num=1
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kn-title=Endothelin-1 production via placental (pro)renin receptor in a mouse model of preeclampsia
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en-aut-name=MISHIMASakurako
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kn-aut-mei=���q
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

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en-title=Pacsin 2�ˑ��I��N-�J�h�w�����̍זE����荞�݂���������̉^���l���𐧌䂷��
kn-title=Pacsin 2-dependent N-cadherin internalization regulates the migration behaviour of malignant cancer cells
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kn-subtitle=
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en-aut-name=WINTHAYMAR
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kn-aut-mei=
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END

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dt-pub-year=2023
dt-pub=20230925
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en-title=���w�Ö@�U���������_�o��Q���f�����b�g�̑O�������ؖ��ɂ�����q�A�������_�����y�f����уq�A�������_�ܗL�זE�̌���
kn-title=Decreased expression of hyaluronan synthase and loss of hyaluronan-rich cells in the anterior tibial fascia of the rat model of chemotherapy-induced peripheral neuropathy
en-subtitle=
kn-subtitle=
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en-copyright=
kn-copyright=

en-aut-name=WANGRUILIN
en-aut-sei=WANG
en-aut-mei=RUILIN
kn-aut-name=������
kn-aut-sei=��
kn-aut-mei=����
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=���R��w��w�@�㎕��w����������
END